By 2010, 35.6 million people are expected to be living with Alzheimer's disease globally, according to Alzheimer's Disease International. The total will probably double every couple of decades and reach approximately 65.7 million by 2030, and 115.4 million twenty years after that, the organization estimates.
Alzheimer's Disease International refers to the current Alzheimer's situation as "an epidemic that is increasing its pace with the graying of the population around the world". It adds that Alzheimer's is poorly recognized, worryingly underdiagnosed, and carries a stigma that causes serious problems for families of patients in all countries, regardless of income levels.
Alzheimer's Disease International recommends that:
WHO (World Health Organization) should declare dementia a world health priority.
Dementia should be declared a health priority by national governments globally. Countries should develop national strategies to provide services and support for patients with dementia, as well as their families.
Dementia strategies should be created by low and medium income countries based first on improving primary healthcare and other community services.
Developed nations should develop national dementia action plans with designated resource allocations.
Services should be developed which take into account the progressive nature of dementia.
Services should be developed and distributed in such a way that coverage is maximized and access is available for everybody. Dementia patients should benefit from services regardless of age, sex, income levels, disability, and where they live.
Government should collaborate, as should caregivers, patients, Alzheimer organizations, and other related NGOs (non-governmental organizations) and professional bodies.
More resources should be channeled towards Alzheimer and other dementia research. There should be more funded research on pharmacological and psychological treatments for Alzheimer's and other dementias - as well as prevention.
What is dementia?
Dementia is the progressive deterioration in cognitive function - the ability to process thought (intelligence).
Progressive means the symptoms will gradually get worse. The deterioration is more than might be expected from normal aging and is due to damage or disease. Damage could be due to a stroke, while an example of a disease might be Alzheimer's.
Dementia is a non-specific syndrome in which different areas of brain function may be affected, including memory, language, problem solving, and attention.
Dementia is not a disease in itself. Alzheimer's is a disease (see below for the difference between Alzheimer's disease and dementia).
When dementia emerges, the higher mental functions of the individual are involved initially. Eventually, during the later stages the patient may not know what day of the week it is, they may not know where they are, and might not be able to identify familiar people around them.
Although dementia is much more common among elderly people, it can affect adults of any age.
What is the difference between Dementia and Alzheimer's Disease?
Alzheimer's disease is a specific disease; dementia is a set of symptoms. Dementia is not a disease.
If you have an infection in your leg, your leg may feel pain. Pain is the symptom and the infection is the disease.
During the course of the Alzheimer's disease plaques and tangles develop within the structure of the brain. This causes brain cells to die. Patients with Alzheimer's also have a deficiency in the levels of some vital brain chemicals which are involved with the transmission of messages in the brain - neurotransmitters.
Alzheimer's disease is the most common form of dementia. The disease gets worse as it develops - it is a progressive disease. There is no current cure for Alzheimer's, although there are ways of slowing down its advance and helping patients with some of the symptoms. Alzheimer's is also a terminal disease - it is incurable and causes death.
According the National Institute on Aging, there are estimated to be between 2.4 million and 4.5 million Americans who have Alzheimer's. There are approximately 417,000 people in the UK with Alzheimer's, according to the Alzheimer's Society.
Dementia can be caused by:
Alzheimer's disease - This is by far the most common cause of dementia. The chemistry and structure of the brain of a person with Alzheimer's disease changes and his brain cells die prematurely.
Stroke (Vascular problems) - this means problems with blood vessels (veins and arteries). Our brain needs a good supply of oxygen-rich blood. If this supply is undermined in any way our brain cells could die - causing symptoms of vascular dementia. Symptoms may appear suddenly, or gradually. A major stroke will cause symptoms to appear suddenly while a series of mini strokes will not.
Dementia with Lewy bodies - spherical structures develop inside nerve cells. Brain cells are nerve cells; they form part of our nervous system. These spherical structures in the brain damage brain tissue. The patient's memory, concentration and ability to speak are affected. Dementia with Lewy bodies is sometimes mistaken for Parkinson's disease because the symptoms are fairly similar.
Fronto-temporal dementia - this includes Pick's disease. The front part of the brain is damaged. The patient's behavior and personality are affected first, later his memory changes.
Other diseases - progressive supranuclear palsy, Korsakoff's syndrome, Binswanger's disease, HIV and AIDS, and Creutzfeldt-Jakob disease (CJD). Dementia is also more common among patients who suffer from Parkinson's disease, Huntington's disease, Motor Neuron disease and Multiple Sclerosis. People who suffer from AIDS sometimes go on to develop cognitive impairment.
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воскресенье, 31 июля 2011 г.
четверг, 28 июля 2011 г.
Second-Hand Smoke Could Cause Dementia
Exposure to second-hand smoke could increase the risk of developing dementia and other forms of cognitive impairment, according to research published today on bmj.
A possible link between active smoking and cognitive impairment has already been established and previous findings also suggest that second-hand smoke exposure could be linked to poor cognitive performance in children and adolescents. However, this is the first large-scale study to conclude that second-hand smoke exposure could lead to dementia and other neurological problems.
The authors, Dr David Llewellyn and his research team from the University of Cambridge, Peninsula Medical School and the University of Michigan, examined saliva samples from almost 5000 non-smoking adults over the age of 50 using data from the 1998, 1999 and 2001 waves of the Health Survey for England (HSE). The participants had also taken part in the English Longitudinal Study of Ageing (ELSA).
The samples were tested for cotinine - a product of nicotine that can be found in saliva for about 25 hours after exposure to second-hand smoke. Participants in the study also provided a detailed smoking history. Never smokers and previous smokers were assessed separately.
The researchers used established neuropsychological tests to assess brain function and cognitive impairment. These focused on memory function, numeracy and verbal fluency - for example naming as many animals in a minute. The results of the tests were added together to provide a global cognitive function score.
Participants whose scores were in the lowest 10% were defined as suffering from some level of cognitive impairment.
The authors argue that the link between second-hand smoke and cognitive impairment could be explained given that heart disease increases the risk of developing dementia and second-hand smoke exposure is known to cause heart disease.
In an accompanying editorial, Dr Mark Eisner from the University of California, says that while the serious negative health effects of second-hand smoke like cancer and premature death have been established beyond doubt, there is still a lot to learn about the scale of illness caused by second-hand smoke.
He writes: "Emerging evidence suggests that parental smoking may impair childhood cognitive development. Later in life, second-hand smoke may cause cardiovascular disease and stroke, which are themselves linked to cognitive decline. Until now, however, the suspicion that passive smoking is bad for the adult brain had not been scientifically confirmed."
Eisner concludes by hoping that greater public awareness about the dangers of second-hand smoke, especially awareness about a much feared disease like dementia, "would eventually translate into political action aimed at passing smoke-free legislation in regions of the world where public smoking is still permitted."
Research: Exposure to second-hand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement, BMJ online
Editorial: Passive smoking and cognitive impairment,
BMJ online
British Medical Journal
A possible link between active smoking and cognitive impairment has already been established and previous findings also suggest that second-hand smoke exposure could be linked to poor cognitive performance in children and adolescents. However, this is the first large-scale study to conclude that second-hand smoke exposure could lead to dementia and other neurological problems.
The authors, Dr David Llewellyn and his research team from the University of Cambridge, Peninsula Medical School and the University of Michigan, examined saliva samples from almost 5000 non-smoking adults over the age of 50 using data from the 1998, 1999 and 2001 waves of the Health Survey for England (HSE). The participants had also taken part in the English Longitudinal Study of Ageing (ELSA).
The samples were tested for cotinine - a product of nicotine that can be found in saliva for about 25 hours after exposure to second-hand smoke. Participants in the study also provided a detailed smoking history. Never smokers and previous smokers were assessed separately.
The researchers used established neuropsychological tests to assess brain function and cognitive impairment. These focused on memory function, numeracy and verbal fluency - for example naming as many animals in a minute. The results of the tests were added together to provide a global cognitive function score.
Participants whose scores were in the lowest 10% were defined as suffering from some level of cognitive impairment.
The authors argue that the link between second-hand smoke and cognitive impairment could be explained given that heart disease increases the risk of developing dementia and second-hand smoke exposure is known to cause heart disease.
In an accompanying editorial, Dr Mark Eisner from the University of California, says that while the serious negative health effects of second-hand smoke like cancer and premature death have been established beyond doubt, there is still a lot to learn about the scale of illness caused by second-hand smoke.
He writes: "Emerging evidence suggests that parental smoking may impair childhood cognitive development. Later in life, second-hand smoke may cause cardiovascular disease and stroke, which are themselves linked to cognitive decline. Until now, however, the suspicion that passive smoking is bad for the adult brain had not been scientifically confirmed."
Eisner concludes by hoping that greater public awareness about the dangers of second-hand smoke, especially awareness about a much feared disease like dementia, "would eventually translate into political action aimed at passing smoke-free legislation in regions of the world where public smoking is still permitted."
Research: Exposure to second-hand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement, BMJ online
Editorial: Passive smoking and cognitive impairment,
BMJ online
British Medical Journal
понедельник, 25 июля 2011 г.
IOS Press Presents Commemorative Volume On Alzheimer's Disease To Her Majesty, Queen Sofia Of Spain
During the recent International Conference on Alzheimer's Disease and Related Disorders (ICAD), IOS Press was honored to present Queen Sofia of Spain with a commemorative edition of Alzheimer's Disease: A Century of Scientific and Clinical Research. This landmark work commemorates the centennial of Alois Alzheimer's discovery of what would be known as Alzheimer's disease (AD). Each conference participant received a copy of the book with the compliments of GlaxoSmithKline.
Through her Queen Sofia Foundation, the Alzheimer's Project, a care and research facility being built in Madrid, will provide inpatient, outpatient, and family services for families that have to deal with Alzheimer's Disease The book traces how the true importance of AD as the major cause of late life dementia ultimately came to light and narrates the evolution of the concepts related to AD throughout the years and its recognition as a major public health problem, with an estimated 30-40 million people affected by AD today. This milestone work has been guided by four of the most prominent voices in the field today, George Perry, Dean of the University of Texas at San Antonio College of Sciences and Professor of Pathology and Neurosciences, Case Western Reserve University, Editor-in-Chief, Journal of Alzheimer's Disease; Jes?s Avila, Center for Molecular Biology, University Aut?noma of Madrid, Senior Editor, Journal of Alzheimer's Disease; June Kinoshita, Executive Editor, Alzheimer Research Forum; and Mark A. Smith, Department of Pathology, Case Western Reserve University, Co-Editor-in-Chief, Journal of Alzheimer's Disease.
George Perry commented, "The book brings to life, and in many instances revisits and reflects on, the classic studies that have essentially defined Alzheimer's disease research. My co-editors and I are extremely pleased that this project has attracted participation from nearly every single player in the field and, having read each contribution and now received feedback from readers, I am convinced that the book is destined to become one of the defining works in the field."
According to Dr. Perry, "These writings bring to the practitioner, student and interested lay person a perspective not only on the past, but also on where the Alzheimer's disease field is likely to go in the future. Only time will tell whether these milestones have charted the future accurately, but they are unquestionably the foundation upon which the future will be built."
About the IOS PRESS BV
IOS Press (iospress.nl) publishes some 70 international journals, ranging from computer science and mathematics to medicine and the natural sciences around 100 book titles a year. Commencing its publishing activities in 1987, IOS Press services a variety of scientific and medical communities in all parts of the world. IOS Press is a fast growing publishing company, which follows the developments in publishing closely. All journals are available online and an online book platform is introduced in 2006. Following its founding, IOS Press established several co-publishing initiatives. Its most recent expansion is the acquisition of the Delft University Press at the end of 2005. IOS Press also maintains offices in the Washington, DC, area, Berlin and a co-publishing relationship with Ohmsha, Ltd (Tokyo).
IOS PRESS BV
Nieuwe Hemweg 6B
iospress.nl
Through her Queen Sofia Foundation, the Alzheimer's Project, a care and research facility being built in Madrid, will provide inpatient, outpatient, and family services for families that have to deal with Alzheimer's Disease The book traces how the true importance of AD as the major cause of late life dementia ultimately came to light and narrates the evolution of the concepts related to AD throughout the years and its recognition as a major public health problem, with an estimated 30-40 million people affected by AD today. This milestone work has been guided by four of the most prominent voices in the field today, George Perry, Dean of the University of Texas at San Antonio College of Sciences and Professor of Pathology and Neurosciences, Case Western Reserve University, Editor-in-Chief, Journal of Alzheimer's Disease; Jes?s Avila, Center for Molecular Biology, University Aut?noma of Madrid, Senior Editor, Journal of Alzheimer's Disease; June Kinoshita, Executive Editor, Alzheimer Research Forum; and Mark A. Smith, Department of Pathology, Case Western Reserve University, Co-Editor-in-Chief, Journal of Alzheimer's Disease.
George Perry commented, "The book brings to life, and in many instances revisits and reflects on, the classic studies that have essentially defined Alzheimer's disease research. My co-editors and I are extremely pleased that this project has attracted participation from nearly every single player in the field and, having read each contribution and now received feedback from readers, I am convinced that the book is destined to become one of the defining works in the field."
According to Dr. Perry, "These writings bring to the practitioner, student and interested lay person a perspective not only on the past, but also on where the Alzheimer's disease field is likely to go in the future. Only time will tell whether these milestones have charted the future accurately, but they are unquestionably the foundation upon which the future will be built."
About the IOS PRESS BV
IOS Press (iospress.nl) publishes some 70 international journals, ranging from computer science and mathematics to medicine and the natural sciences around 100 book titles a year. Commencing its publishing activities in 1987, IOS Press services a variety of scientific and medical communities in all parts of the world. IOS Press is a fast growing publishing company, which follows the developments in publishing closely. All journals are available online and an online book platform is introduced in 2006. Following its founding, IOS Press established several co-publishing initiatives. Its most recent expansion is the acquisition of the Delft University Press at the end of 2005. IOS Press also maintains offices in the Washington, DC, area, Berlin and a co-publishing relationship with Ohmsha, Ltd (Tokyo).
IOS PRESS BV
Nieuwe Hemweg 6B
iospress.nl
пятница, 22 июля 2011 г.
Alzheimer's Society Comment On Department Of Health Announcement On National Strategy For Dementia, UK
Today is a pivotal moment for millions of families affected by dementia. For too long dementia has been at the bottom of health and social care pile. This announcement by our new government represents a real step forward in policy towards dementia.
Dementia is the health and social care challenge of the century. This is an exciting opportunity to make sure the knowledge and expertise we now have about dementia care and treatment makes a difference to the lives of thousands of people throughout England.
There is a huge task ahead. Currently, 600,000 people have dementia in England yet more than half of these will never receive a formal diagnosis and families are often left to cope alone until they reach crisis point. In less than twenty years over a million people will have dementia, we look forward to working with the government to ensure people now and in the future receive the care and support they deserve.
-- Alzheimer's is a progressive disease that causes a person's ability to remember, understand, communicate and reason to decline. It is the most common form of dementia.
-- 1 in 3 older people will end their life with dementia.
-- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 5 people over 80 have dementia.
-- The Alzheimer's Society champions the rights of people living with dementia and those who care for them. The Alzheimer's Society works in England, Wales and Northern Ireland.
-- As a charity, the Alzheimer's Society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now visiting alzheimers.uk.
Dementia is the health and social care challenge of the century. This is an exciting opportunity to make sure the knowledge and expertise we now have about dementia care and treatment makes a difference to the lives of thousands of people throughout England.
There is a huge task ahead. Currently, 600,000 people have dementia in England yet more than half of these will never receive a formal diagnosis and families are often left to cope alone until they reach crisis point. In less than twenty years over a million people will have dementia, we look forward to working with the government to ensure people now and in the future receive the care and support they deserve.
-- Alzheimer's is a progressive disease that causes a person's ability to remember, understand, communicate and reason to decline. It is the most common form of dementia.
-- 1 in 3 older people will end their life with dementia.
-- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 5 people over 80 have dementia.
-- The Alzheimer's Society champions the rights of people living with dementia and those who care for them. The Alzheimer's Society works in England, Wales and Northern Ireland.
-- As a charity, the Alzheimer's Society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now visiting alzheimers.uk.
вторник, 19 июля 2011 г.
Reversing Abnormal Brain Activity In Alzheimer Models Improves Development Of New Nerve Cells Born In Adult Brains
Stimulating the growth of new neurons to replace those lost in Alzheimer's disease (AD) is an intriguing therapeutic possibility. But will the factors that cause AD allow the new neurons to thrive and function normally? Scientists at the Gladstone Institute of Neurological Disease (GIND) have discovered that two main causes of AD amyloid-beta (A??) peptides and apolipoprotein E4 (apoE4) impair the growth of new neurons born in adult brains. What is more, they have identified drug treatments that can normalize the development of these cells even in the presence of A?? or apoE4. The findings are described in two separate papers published in the current issue of Cell Stem Cell.
Although it had long been assumed that neurons cannot be renewed, it is now well established that new neurons are generated throughout the lives of mammals. One brain region in which new neurons are born in adults, the hippocampus, is involved in learning and memory and affected severely by Alzheimer's disease.
GIND investigator Li Gan, PhD, and her collaborators studied the development of neurons born in the hippocampus of adult mice genetically engineered to produce high levels of human A?? in the brain. Surprisingly, A?? initially accelerated the development of newborn neurons but then profoundly impaired their maturation at later stages of development.
"Interestingly," Dr. Gan said, "we were able to protect the newborn neurons and ensure their normal development with drugs that counteract A??-induced abnormalities in neural network activity. It is possible that these drugs could support the development of neurons from stem cells even in the hostile environment of the AD brain."
In a complementary study, GIND investigator Yadong Huang, MD, PhD and his team focused on apoE4, the major genetic risk factor for AD. The team used genetically engineered mice to study the effects of different human apoE variants on the maturation of neural stem cells or progenitor cells, from which new neurons develop in the adult brain. They found that apoE4 also impairs the development of new neurons in the hippocampus and identified drug treatments that could block these detrimental effects.
"Our findings suggest that apoE4 inhibits the development of newborn neurons by impairing specific signaling pathways and that boosting these pathways with drugs may be of therapeutic benefit," said Dr. Huang. "It might allow us to encourage the development of new neurons from stem cells to replace those lost in apoE4 carriers with AD."
"Although stem cell therapy for AD is still a long ways off, these studies have identified strategies to overcome major obstacles in the path towards this goal," said GIND Director Lennart Mucke, MD, who coauthored one of the studies. "They clearly demonstrate that drugs can be used to improve the development of newborn neurons in memory centers of the adult brain, even in the presence of toxic factors widely presumed to cause AD."
Dr. Gan's research was supported by the J. David Gladstone Institutes and the L.K.Whittier Foundation. Binggui Sun, Brian Halabisky, Yungui Zhou, Jorge Palop, Guiqiu Yu, and Lennart Mucke also contributed to this research. Dr. Huang's research was supported by the J. David Gladstone Institutes, the California Institute for Regenerative Medicine, and the National Institutes of Health. Gang Li, Nga Bien-Ly, Yaisa Andrews-Zwilling, Aubrey Bernardo, Karen Ring, Brian Halabisky, Changhui Deng, and Robert W. Mahley also contributed to this research.
Dr. Gan's and Dr. Huang's primary affiliations are with the Gladstone Institute of Neurological Disease where their laboratories are located and all of their research is conducted. Dr. Gan is also Assistant Professor of Neurology and Dr. Huang is Associate Professor of Pathology and Neurology at the University of California, San Francisco.
In addition to his primary affiliation as Director of the Gladstone Institute of Neurological Disease, Dr. Mucke is the Joseph B. Martin Distinguished Professor of Neuroscience and Professor of Neurology at the University of California, San Francisco.
Source: Valerie Tucker
Gladstone Institutes
Although it had long been assumed that neurons cannot be renewed, it is now well established that new neurons are generated throughout the lives of mammals. One brain region in which new neurons are born in adults, the hippocampus, is involved in learning and memory and affected severely by Alzheimer's disease.
GIND investigator Li Gan, PhD, and her collaborators studied the development of neurons born in the hippocampus of adult mice genetically engineered to produce high levels of human A?? in the brain. Surprisingly, A?? initially accelerated the development of newborn neurons but then profoundly impaired their maturation at later stages of development.
"Interestingly," Dr. Gan said, "we were able to protect the newborn neurons and ensure their normal development with drugs that counteract A??-induced abnormalities in neural network activity. It is possible that these drugs could support the development of neurons from stem cells even in the hostile environment of the AD brain."
In a complementary study, GIND investigator Yadong Huang, MD, PhD and his team focused on apoE4, the major genetic risk factor for AD. The team used genetically engineered mice to study the effects of different human apoE variants on the maturation of neural stem cells or progenitor cells, from which new neurons develop in the adult brain. They found that apoE4 also impairs the development of new neurons in the hippocampus and identified drug treatments that could block these detrimental effects.
"Our findings suggest that apoE4 inhibits the development of newborn neurons by impairing specific signaling pathways and that boosting these pathways with drugs may be of therapeutic benefit," said Dr. Huang. "It might allow us to encourage the development of new neurons from stem cells to replace those lost in apoE4 carriers with AD."
"Although stem cell therapy for AD is still a long ways off, these studies have identified strategies to overcome major obstacles in the path towards this goal," said GIND Director Lennart Mucke, MD, who coauthored one of the studies. "They clearly demonstrate that drugs can be used to improve the development of newborn neurons in memory centers of the adult brain, even in the presence of toxic factors widely presumed to cause AD."
Dr. Gan's research was supported by the J. David Gladstone Institutes and the L.K.Whittier Foundation. Binggui Sun, Brian Halabisky, Yungui Zhou, Jorge Palop, Guiqiu Yu, and Lennart Mucke also contributed to this research. Dr. Huang's research was supported by the J. David Gladstone Institutes, the California Institute for Regenerative Medicine, and the National Institutes of Health. Gang Li, Nga Bien-Ly, Yaisa Andrews-Zwilling, Aubrey Bernardo, Karen Ring, Brian Halabisky, Changhui Deng, and Robert W. Mahley also contributed to this research.
Dr. Gan's and Dr. Huang's primary affiliations are with the Gladstone Institute of Neurological Disease where their laboratories are located and all of their research is conducted. Dr. Gan is also Assistant Professor of Neurology and Dr. Huang is Associate Professor of Pathology and Neurology at the University of California, San Francisco.
In addition to his primary affiliation as Director of the Gladstone Institute of Neurological Disease, Dr. Mucke is the Joseph B. Martin Distinguished Professor of Neuroscience and Professor of Neurology at the University of California, San Francisco.
Source: Valerie Tucker
Gladstone Institutes
суббота, 16 июля 2011 г.
Baxter And The Alzheimer's Disease Cooperative Study Group To Pursue A Phase III Study Of Gammagard Liquid In Patients With Alzheimer's Disease
Baxter International
Inc. (NYSE: BAX) and The Alzheimer's Disease Cooperative Study (ADCS) group
today announced the decision to pursue a multi-center U.S. Phase III study
evaluating the role of Gammagard Liquid [Immune Globulin Intravenous
(Human)] (IGIV), an intravenous immunoglobulin preparation, for the
treatment of patients with mild to moderate alzheimer's disease. GAMMAGARD
Liquid contains a broad spectrum of immunoglobulins (antibodies), and is
indicated as an immunoglobulin replacement therapy in patients with primary
immunodeficiency.
GAMMAGARD Liquid is processed from large pools of human plasma. IGIV
has been used for almost three decades to treat primary immunodeficiency.
IGIV is not currently approved for the treatment of Alzheimer's disease,
and to date has not been established to be effective in this indication.
The rationale for testing IGIV as a possible treatment for Alzheimer's is
based on the presence of natural antibodies that are directed against
several forms of beta amyloid. Beta amyloid is a protein found in plaques
that accumulate in the brains of patients with Alzheimer's disease, and is
considered to play a key role in the cognitive decline observed in these
patients. Treatment with naturally occurring antibodies against beta
amyloid contained in IGIV may result in clearance of beta amyloid from the
brain and dissolution of plaques.
The decision to pursue the Phase III study is based on the results of
two completed open-label clinical studies, and the preliminary analysis of
interim data from a double-blind, placebo-controlled phase II study by Dr.
Norman Relkin and his colleagues at Weill Cornell Medical College in New
York City. In this study, 24 patients with mild to moderate Alzheimer's
disease were randomly assigned to receive GAMMAGARD Liquid, GAMMAGARD S/D
or placebo (eight patients were treated with GAMMAGARD Liquid, eight
patients were treated with GAMMAGARD S/D and eight patients received
placebo) for six months. Cognitive, behavioral and functional measures were
collected at baseline, three months and six months of treatment. The
primary endpoints of the Phase II trial were cognitive function (as
measured by ADAS-Cog score) and global function (as assessed by ADCS-CGIC
rating). The pre-specified criterion for going forward with Phase III was a
favorable outcome in IGIV-treated patients relative to those given placebo.
Final results of the analysis of the Phase II study are expected later this
year.
The Phase II study follows Dr. Relkin's earlier Phase I results in
eight patients that were reported at the International Conference on
Alzheimer's Disease in Madrid in July, 2006. Although these findings are
promising, both studies were small and results must therefore be confirmed
in a larger, sufficiently powered study.
The study protocol will be submitted to the U.S. Food and Drug
Administration for review in the coming months with the intention of
initiating patient recruitment early in 2008. The ADCS Phase III trial is
sponsored jointly by the National Institutes of Health and Baxter. The
trial will include approximately 35 leading academic centers in the U.S.
that are members of ADCS.
GAMMAGARD LIQUID
[Immune Globulin Intravenous (Human)] 10% GAMMAGARD LIQUID is indicated for the treatment of primary immunodeficiency disorders associated with defects in humoral immunity. These include but are not limited to congenital X-linked
agammaglobulinemia, common variable immunodeficiency, Wiskott-Aldrich
syndrome, and severe combined immunodeficiencies.
Important Safety Information
GAMMAGARD LIQUID is contraindicated in patients with known anaphylactic
or severe hypersensitivity responses to Immune Globulin (Human). Patients
with severe selective IgA deficiency (IgA < 0.05 g/L) may develop anti-IgA
antibodies that can result in a severe anaphylactic reaction.
Immune Globulin Intravenous (Human) products have been reported to be
associated with renal dysfunction, acute renal failure, osmotic nephrosis,
and death. Patients predisposed to acute renal failure include patients
with any degree of pre-existing renal insufficiency, diabetes mellitus,
age greater than 65, volume depletion, sepsis, paraproteinemia, or
patients receiving known nephrotoxic drugs. Especially in such patients,
IGIV products should be administered at the minimum concentration
available and the minimum rate of infusion practicable. While these
reports of renal dysfunction and acute renal failure have been associated
with the use of many of the licensed IGIV products, those containing
sucrose as a stabilizer accounted for a disproportionate share of the
total number.
Glycine, an amino acid, is used as a stabilizer. GAMMAGARD
LIQUID does not contain sucrose.
GAMMAGARD LIQUID is made from human plasma. It may carry a risk of
transmitting infectious agents, e.g. viruses, and theoretically, the
Creutzfeldt-Jakob disease (CJD) agent.
Components used in the packaging of this product are latex-free.
Thrombotic events have been reported in association with IGIV. Patients
at risk may include those with a history of atherosclerosis, multiple
cardiovascular risk factors, advanced age, impaired cardiac output, and/or
known or suspected hyperviscosity, hypercoagulable disorders, and prolonged
periods of immobilization.
IGIV products can contain blood group antibodies that may cause a
positive direct antiglobulin reaction and, rarely, hemolysis.
Aseptic meningitis syndrome (AMS) has been reported to occur
infrequently in association with IGIV treatment. Discontinuation of IGIV
treatment has resulted in remission of AMS within several days without
sequelae.
Various mild and moderate reactions, such as headache, fever, fatigue,
chills, flushing, dizziness, urticaria, wheezing or chest tightness,
nausea, vomiting, rigors, back pain, chest pain, muscle cramps, and changes
in blood pressure may occur with infusions of Immune Globulin Intravenous
(Human).
GAMMAGARD S/D
[Immune Globulin Intravenous (Human)]
GAMMAGARD S/D is indicated for the treatment of primary
immunodeficiency disorders associated with defects in humoral immunity.
These include but are not limited to congenital X-linked
agammaglobulinemia, common variable immunodeficiency, Wiskott-Aldrich
syndrome, and severe combined immunodeficiencies.
GAMMAGARD S/D must not be used in patients with selective IgA
deficiency (IgA, 0.05 g/L) where the IgA deficiency is the only abnormality
of concern.
Important Safety Information
Patients may experience severe hypersensitivity reactions or
anaphylaxis in the setting of detectable IgA levels following infusion of
GAMMAGARD S/D.
Immune Globulin Intravenous (Human) products have been reported to be
associated with renal dysfunction, acute renal failure, osmotic nephrosis,
and death. Patients predisposed to acute renal failure include patients
with any degree of pre-existing renal insufficiency, diabetes mellitus,
age greater than 65, volume depletion, sepsis, paraproteinemia, or
patients receiving known nephrotoxic drugs. Especially in such patients,
IGIV products should be administered at the minimum concentration
available and the minimum rate of infusion practicable. While these
reports of renal dysfunction and acute renal failure have been associated
with the use of many of the licensed IGIV products, those containing
sucrose as a stabilizer accounted for a disproportionate share of the
total number.
GAMMAGARD S/D does not contain sucrose.
GAMMAGARD S/D is made from human plasma. It may carry a risk of
transmitting infectious agents, e.g. viruses, and theoretically, the
Creutzfeldt-Jakob disease (CJD) agent.
Aseptic meningitis syndrome (AMS) has been reported to occur
infrequently in association with IGIV treatment. Discontinuation of IGIV
treatment has resulted in remission of AMS within several days without
sequelae.
Certain components used in the packaging of GAMMAGARD S/D contain
natural rubber latex.
IGIV products can contain blood group antibodies that may cause a
positive direct antiglobulin reaction and, rarely, hemolysis.
Thrombotic events have been reported in association with IGIV. Patients
at risk may include those with a history of atherosclerosis, multiple
cardiovascular risk factors, advanced age, impaired cardiac output, and/or
known or suspected hyperviscosity, hypercoagulable disorders, and prolonged
periods of immobilization.
Various minor reactions, such as mild to moderate hypotension,
headache, fatigue, chills, backache, leg cramps, lightheadedness, fever,
urticaria, flushing, slight elevation of blood pressure, nausea and
vomiting, may occasionally occur.
Baxter International Inc., through its subsidiaries, assists healthcare
professionals and their patients with the treatment of complex medical
conditions, including hemophilia, immune disorders, cancer, infectious
diseases, kidney disease, trauma and other conditions. The company applies
its expertise in medical devices, pharmaceuticals and biotechnology to make
a meaningful difference in patients' lives.
This release includes forward-looking statements concerning IGIV
relating to clinical trials and their timing, as well as potential future
uses of the product. The statements are based on assumptions about many
important factors, including the following, which could cause actual
results to differ materially from those in the forward-looking statements:
continuing review of preliminary trial data and the limited number of
patients studied to date; additional regulatory and other steps required
prior to the initiation of the larger study described in the release; and
other risks identified in the company's most recent filing on Form 10-Q and
other SEC filings, all of which are available on the company's web site.
The company does not undertake to update its forward-looking statements.
Baxter International Inc.
baxter
Inc. (NYSE: BAX) and The Alzheimer's Disease Cooperative Study (ADCS) group
today announced the decision to pursue a multi-center U.S. Phase III study
evaluating the role of Gammagard Liquid [Immune Globulin Intravenous
(Human)] (IGIV), an intravenous immunoglobulin preparation, for the
treatment of patients with mild to moderate alzheimer's disease. GAMMAGARD
Liquid contains a broad spectrum of immunoglobulins (antibodies), and is
indicated as an immunoglobulin replacement therapy in patients with primary
immunodeficiency.
GAMMAGARD Liquid is processed from large pools of human plasma. IGIV
has been used for almost three decades to treat primary immunodeficiency.
IGIV is not currently approved for the treatment of Alzheimer's disease,
and to date has not been established to be effective in this indication.
The rationale for testing IGIV as a possible treatment for Alzheimer's is
based on the presence of natural antibodies that are directed against
several forms of beta amyloid. Beta amyloid is a protein found in plaques
that accumulate in the brains of patients with Alzheimer's disease, and is
considered to play a key role in the cognitive decline observed in these
patients. Treatment with naturally occurring antibodies against beta
amyloid contained in IGIV may result in clearance of beta amyloid from the
brain and dissolution of plaques.
The decision to pursue the Phase III study is based on the results of
two completed open-label clinical studies, and the preliminary analysis of
interim data from a double-blind, placebo-controlled phase II study by Dr.
Norman Relkin and his colleagues at Weill Cornell Medical College in New
York City. In this study, 24 patients with mild to moderate Alzheimer's
disease were randomly assigned to receive GAMMAGARD Liquid, GAMMAGARD S/D
or placebo (eight patients were treated with GAMMAGARD Liquid, eight
patients were treated with GAMMAGARD S/D and eight patients received
placebo) for six months. Cognitive, behavioral and functional measures were
collected at baseline, three months and six months of treatment. The
primary endpoints of the Phase II trial were cognitive function (as
measured by ADAS-Cog score) and global function (as assessed by ADCS-CGIC
rating). The pre-specified criterion for going forward with Phase III was a
favorable outcome in IGIV-treated patients relative to those given placebo.
Final results of the analysis of the Phase II study are expected later this
year.
The Phase II study follows Dr. Relkin's earlier Phase I results in
eight patients that were reported at the International Conference on
Alzheimer's Disease in Madrid in July, 2006. Although these findings are
promising, both studies were small and results must therefore be confirmed
in a larger, sufficiently powered study.
The study protocol will be submitted to the U.S. Food and Drug
Administration for review in the coming months with the intention of
initiating patient recruitment early in 2008. The ADCS Phase III trial is
sponsored jointly by the National Institutes of Health and Baxter. The
trial will include approximately 35 leading academic centers in the U.S.
that are members of ADCS.
GAMMAGARD LIQUID
[Immune Globulin Intravenous (Human)] 10% GAMMAGARD LIQUID is indicated for the treatment of primary immunodeficiency disorders associated with defects in humoral immunity. These include but are not limited to congenital X-linked
agammaglobulinemia, common variable immunodeficiency, Wiskott-Aldrich
syndrome, and severe combined immunodeficiencies.
Important Safety Information
GAMMAGARD LIQUID is contraindicated in patients with known anaphylactic
or severe hypersensitivity responses to Immune Globulin (Human). Patients
with severe selective IgA deficiency (IgA < 0.05 g/L) may develop anti-IgA
antibodies that can result in a severe anaphylactic reaction.
Immune Globulin Intravenous (Human) products have been reported to be
associated with renal dysfunction, acute renal failure, osmotic nephrosis,
and death. Patients predisposed to acute renal failure include patients
with any degree of pre-existing renal insufficiency, diabetes mellitus,
age greater than 65, volume depletion, sepsis, paraproteinemia, or
patients receiving known nephrotoxic drugs. Especially in such patients,
IGIV products should be administered at the minimum concentration
available and the minimum rate of infusion practicable. While these
reports of renal dysfunction and acute renal failure have been associated
with the use of many of the licensed IGIV products, those containing
sucrose as a stabilizer accounted for a disproportionate share of the
total number.
Glycine, an amino acid, is used as a stabilizer. GAMMAGARD
LIQUID does not contain sucrose.
GAMMAGARD LIQUID is made from human plasma. It may carry a risk of
transmitting infectious agents, e.g. viruses, and theoretically, the
Creutzfeldt-Jakob disease (CJD) agent.
Components used in the packaging of this product are latex-free.
Thrombotic events have been reported in association with IGIV. Patients
at risk may include those with a history of atherosclerosis, multiple
cardiovascular risk factors, advanced age, impaired cardiac output, and/or
known or suspected hyperviscosity, hypercoagulable disorders, and prolonged
periods of immobilization.
IGIV products can contain blood group antibodies that may cause a
positive direct antiglobulin reaction and, rarely, hemolysis.
Aseptic meningitis syndrome (AMS) has been reported to occur
infrequently in association with IGIV treatment. Discontinuation of IGIV
treatment has resulted in remission of AMS within several days without
sequelae.
Various mild and moderate reactions, such as headache, fever, fatigue,
chills, flushing, dizziness, urticaria, wheezing or chest tightness,
nausea, vomiting, rigors, back pain, chest pain, muscle cramps, and changes
in blood pressure may occur with infusions of Immune Globulin Intravenous
(Human).
GAMMAGARD S/D
[Immune Globulin Intravenous (Human)]
GAMMAGARD S/D is indicated for the treatment of primary
immunodeficiency disorders associated with defects in humoral immunity.
These include but are not limited to congenital X-linked
agammaglobulinemia, common variable immunodeficiency, Wiskott-Aldrich
syndrome, and severe combined immunodeficiencies.
GAMMAGARD S/D must not be used in patients with selective IgA
deficiency (IgA, 0.05 g/L) where the IgA deficiency is the only abnormality
of concern.
Important Safety Information
Patients may experience severe hypersensitivity reactions or
anaphylaxis in the setting of detectable IgA levels following infusion of
GAMMAGARD S/D.
Immune Globulin Intravenous (Human) products have been reported to be
associated with renal dysfunction, acute renal failure, osmotic nephrosis,
and death. Patients predisposed to acute renal failure include patients
with any degree of pre-existing renal insufficiency, diabetes mellitus,
age greater than 65, volume depletion, sepsis, paraproteinemia, or
patients receiving known nephrotoxic drugs. Especially in such patients,
IGIV products should be administered at the minimum concentration
available and the minimum rate of infusion practicable. While these
reports of renal dysfunction and acute renal failure have been associated
with the use of many of the licensed IGIV products, those containing
sucrose as a stabilizer accounted for a disproportionate share of the
total number.
GAMMAGARD S/D does not contain sucrose.
GAMMAGARD S/D is made from human plasma. It may carry a risk of
transmitting infectious agents, e.g. viruses, and theoretically, the
Creutzfeldt-Jakob disease (CJD) agent.
Aseptic meningitis syndrome (AMS) has been reported to occur
infrequently in association with IGIV treatment. Discontinuation of IGIV
treatment has resulted in remission of AMS within several days without
sequelae.
Certain components used in the packaging of GAMMAGARD S/D contain
natural rubber latex.
IGIV products can contain blood group antibodies that may cause a
positive direct antiglobulin reaction and, rarely, hemolysis.
Thrombotic events have been reported in association with IGIV. Patients
at risk may include those with a history of atherosclerosis, multiple
cardiovascular risk factors, advanced age, impaired cardiac output, and/or
known or suspected hyperviscosity, hypercoagulable disorders, and prolonged
periods of immobilization.
Various minor reactions, such as mild to moderate hypotension,
headache, fatigue, chills, backache, leg cramps, lightheadedness, fever,
urticaria, flushing, slight elevation of blood pressure, nausea and
vomiting, may occasionally occur.
Baxter International Inc., through its subsidiaries, assists healthcare
professionals and their patients with the treatment of complex medical
conditions, including hemophilia, immune disorders, cancer, infectious
diseases, kidney disease, trauma and other conditions. The company applies
its expertise in medical devices, pharmaceuticals and biotechnology to make
a meaningful difference in patients' lives.
This release includes forward-looking statements concerning IGIV
relating to clinical trials and their timing, as well as potential future
uses of the product. The statements are based on assumptions about many
important factors, including the following, which could cause actual
results to differ materially from those in the forward-looking statements:
continuing review of preliminary trial data and the limited number of
patients studied to date; additional regulatory and other steps required
prior to the initiation of the larger study described in the release; and
other risks identified in the company's most recent filing on Form 10-Q and
other SEC filings, all of which are available on the company's web site.
The company does not undertake to update its forward-looking statements.
Baxter International Inc.
baxter
среда, 13 июля 2011 г.
Rote Learning Improves Memory In Seniors
A new study offers older adults a simple way to combat memory loss: memorization. Researchers found that seniors who engaged in an intensive period of rote learning followed by an equally long rest period exhibited improved memory and verbal recall. The study was presented at the annual meeting of the Radiological Society of North America (RSNA).
"We didn't see an immediate improvement following the intensive memorization period," said Jonathan McNulty, B.Sc., H.Dip., of Diagnostic Imaging at the School of Medicine and Medical Science, University College Dublin in Ireland. "However, after a six-week rest, the volunteers manifested both metabolic changes in the brain and improved memory performance."
As people age, they often begin to experience forgetfulness and may have difficulty learning new material. Approximately 40 percent of people over age 60 have some kind of memory difficulty. Mild, age-related memory loss is caused by the loss of brain cells over time, along with changes in brain chemistry. The researchers studied how repeated cognitive exercise impacts memory and recall, as well as the health of brain cells involved in memory.
The study involved 24 healthy older adults between the ages of 55 and 70. The volunteers engaged in six weeks of intensive rote learning, memorizing a newspaper article or poem of 500 words, followed by six weeks of rest.
An extensive battery of learning and memory tests was administered before and after the six-week learning period. Magnetic resonance spectroscopy (MRS), a special type of magnetic resonance imaging, was performed on half of the volunteers before and after the intensive learning session, and again six weeks later. MRS was used to measure changes in N-acetylaspartate, creatine and choline, three metabolites in the brain that are related to memory performance and neural cell health.
At the end of the six-week learning session, no changes in the brain metabolism or memory performance were observed. But following the rest period, all of the volunteers experienced improvements in their verbal and episodic memory - they were better able to remember and repeat a short story and a list of words and to recall events that occurred earlier in the day or week. These behavioral changes correlated with metabolic changes identified by MRS in the left posterior hippocampus, a memory-related brain structure.
"Unlike other studies on memory involving specific training regimes, memorizing is an everyday activity that anyone can undertake," said co-author Richard Roche, Ph.D., of the Department of Psychology at National University of Ireland in Maynooth. "The brain is like a muscle that should be exercised through the retirement years as a defense against dementia, cognitive lapses and memory failure."
Co-authors are Paul Brennan, M.D., Colin P. Doherty, M.D., D. McMackin, M.D., S. Sukumaran, M.D., I.H. Robertson, Ph.D., M.A. Mangaoang, Ph.D., S.M. O'Mara, D.Phil., Sinead L. Mullally, Ph.D., J. Hayden, B.A., J. Prendergast, B.Sc., and M. Fitzsimons, Ph.D.
RSNA is an association of more than 40,000 radiologists, radiation oncologists, medical physicists and related scientists committed to promoting excellence in radiology through education and by fostering research, with the ultimate goal of improving patient care. The Society is based in Oak Brook, Ill.
The data in these releases may differ from those in the printed abstract and those actually presented at the meeting, as researchers continue to update their data right up until the meeting.
Contact: Maureen Morley
Radiological Society of North America
"We didn't see an immediate improvement following the intensive memorization period," said Jonathan McNulty, B.Sc., H.Dip., of Diagnostic Imaging at the School of Medicine and Medical Science, University College Dublin in Ireland. "However, after a six-week rest, the volunteers manifested both metabolic changes in the brain and improved memory performance."
As people age, they often begin to experience forgetfulness and may have difficulty learning new material. Approximately 40 percent of people over age 60 have some kind of memory difficulty. Mild, age-related memory loss is caused by the loss of brain cells over time, along with changes in brain chemistry. The researchers studied how repeated cognitive exercise impacts memory and recall, as well as the health of brain cells involved in memory.
The study involved 24 healthy older adults between the ages of 55 and 70. The volunteers engaged in six weeks of intensive rote learning, memorizing a newspaper article or poem of 500 words, followed by six weeks of rest.
An extensive battery of learning and memory tests was administered before and after the six-week learning period. Magnetic resonance spectroscopy (MRS), a special type of magnetic resonance imaging, was performed on half of the volunteers before and after the intensive learning session, and again six weeks later. MRS was used to measure changes in N-acetylaspartate, creatine and choline, three metabolites in the brain that are related to memory performance and neural cell health.
At the end of the six-week learning session, no changes in the brain metabolism or memory performance were observed. But following the rest period, all of the volunteers experienced improvements in their verbal and episodic memory - they were better able to remember and repeat a short story and a list of words and to recall events that occurred earlier in the day or week. These behavioral changes correlated with metabolic changes identified by MRS in the left posterior hippocampus, a memory-related brain structure.
"Unlike other studies on memory involving specific training regimes, memorizing is an everyday activity that anyone can undertake," said co-author Richard Roche, Ph.D., of the Department of Psychology at National University of Ireland in Maynooth. "The brain is like a muscle that should be exercised through the retirement years as a defense against dementia, cognitive lapses and memory failure."
Co-authors are Paul Brennan, M.D., Colin P. Doherty, M.D., D. McMackin, M.D., S. Sukumaran, M.D., I.H. Robertson, Ph.D., M.A. Mangaoang, Ph.D., S.M. O'Mara, D.Phil., Sinead L. Mullally, Ph.D., J. Hayden, B.A., J. Prendergast, B.Sc., and M. Fitzsimons, Ph.D.
RSNA is an association of more than 40,000 radiologists, radiation oncologists, medical physicists and related scientists committed to promoting excellence in radiology through education and by fostering research, with the ultimate goal of improving patient care. The Society is based in Oak Brook, Ill.
The data in these releases may differ from those in the printed abstract and those actually presented at the meeting, as researchers continue to update their data right up until the meeting.
Contact: Maureen Morley
Radiological Society of North America
воскресенье, 10 июля 2011 г.
Impaired clearance of amyloid-beta causes vascular damage in Alzheimer's disease
New research suggests that accumulation of amyloid-?? peptides in cerebral blood vessels, as opposed to the brain itself, may be a more important pathological mediator of Alzheimer's disease. Two independent yet related articles describe such findings in the August issue of The American Journal of Pathology. Both articles are highlighted on the Journal's cover.
Alzheimer's disease, the most common form of progressive dementia, affects an estimated 4.5 million Americans according to the Alzheimer's Association. Amyloid-?? (A??) deposition is a hallmark of Alzheimer's disease and other cerebral amyloid angiopathies. However, exactly how A?? accumulates and causes damage is not fully understood.
In the first article, "Cerebral microvascular A?? deposition induces vascular degeneration and neuroinflammation in transgenic mice expressing human vasculotropic mutant A??PP," Miao et al. describe early-onset A?? deposition in Tg-SwDI mice. These mice express A?? protein with mutations that are found in human early-onset cerebral amyloid angiopathy, causing specific accumulation of A?? in cerebral blood vessels.
The A?? peptides accumulated because they could not adequately cross the blood-brain barrier to be cleared from the brain. Over time, A?? accumulation increased in the cerebral microvessels of the thalamus and subiculum of the brain. This resulted in degeneration of blood vessels as evidenced by reduced vessel density and increased apoptosis. Neuroinflammation also occurred as large numbers of microglia, along with inflammatory cytokines, were found at sites of A?? accumulation.
The authors conclude that early-onset A?? accumulation occurs predominantly in the cerebral microvasculature and appears largely responsible for the neuroinflammation in these mice. They also demonstrate the utility of Tg-SwDI mice in studying cerebral amyloid angiopathies, such as Alzheimer's disease.
The second article, by Kumar-Singh et al., "Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls," utilizes two different transgenic mice: Tg2576 and PSAPP. Both models produce dense-core plaques, highly concentrated deposits of A??, and were used to investigate the possible association of blood vessels with A?? deposits.
In these mice, dense-core plaques associated with cerebral vessels with high specificity. There was also evidence of vessel damage and blood-brain barrier damage, resulting in release of A?? through the vessel walls and accumulation of plaques next to the vessels. These data confirm previous observations in humans that senile plaques associate with blood vessels, especially in the vasculotropic Flemish type of Alzheimer's disease.
The authors propose a model of dense-core plaque formation that is dependent on cerebral vessels. As A?? is cleared from the brain, it exerts a cytotoxic effect on the endothelial cells of the vascular wall (a process that may be exacerbated if clearance is impaired). This leads to loss of vessel integrity and accumulation of A?? in the area surrounding the compromised vessel wall. Eventually, the damage is so great that the blood vessel deteriorates beyond functional use and new vessels form to pick up the slack. The result is a multicentric dense-core plaque that associates with multiple vessels.
These studies describe several animal models for further examining the pathogenesis and treatment of Alzheimer's disease and related cerebral amyloid angiopathies. And both studies confirm that A?? generated by neurons accumulates in blood vessels following attempted clearance of excess A?? peptides. Thus, study of novel therapies that reduce the blood vessel-associated deposition of A?? may prove beneficial to patients with Alzheimer's disease.
*Miao J, Xu F, Davis J, Otte-H?ller I, Verbeek MM, Van Nostrand WE: Cerebral microvascular A?? deposition induces vascular degeneration and neuroinflammation in transgenic mice expressing human vasculotropic mutant A??PP. Am J Pathol 2005, 167: 505-515
†Kumar-Singh S, Pirici D, McGowan E, Serneels S, Ceuterick C, Hardy J, Duff K, Dickson D, Van Broeckhoven C: Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls. Am J Pathol 2005, 167: 527-543
*Work was performed at Stony Brook University, New York. †Work was performed at the Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
For press copies of the article, please contact Audra Cox at 301-634-7409.
The American Journal of Pathology, the official journal of the American Society for Investigative Pathology (ASIP), seeks to publish high-quality original papers on the cellular and molecular mechanisms of disease. The editors accept manuscripts which report important findings on disease pathogenesis or basic biological mechanisms that relate to disease, without preference for a specific method of analysis. High priority is given to studies on human disease and relevant experimental models using cellular, molecular, biological, animal, chemical and immunological approaches in conjunction with morphology.
Audra Cox
acoxasip
301-634-7409
American Journal of Pathology
ajp.amjpathol
Alzheimer's disease, the most common form of progressive dementia, affects an estimated 4.5 million Americans according to the Alzheimer's Association. Amyloid-?? (A??) deposition is a hallmark of Alzheimer's disease and other cerebral amyloid angiopathies. However, exactly how A?? accumulates and causes damage is not fully understood.
In the first article, "Cerebral microvascular A?? deposition induces vascular degeneration and neuroinflammation in transgenic mice expressing human vasculotropic mutant A??PP," Miao et al. describe early-onset A?? deposition in Tg-SwDI mice. These mice express A?? protein with mutations that are found in human early-onset cerebral amyloid angiopathy, causing specific accumulation of A?? in cerebral blood vessels.
The A?? peptides accumulated because they could not adequately cross the blood-brain barrier to be cleared from the brain. Over time, A?? accumulation increased in the cerebral microvessels of the thalamus and subiculum of the brain. This resulted in degeneration of blood vessels as evidenced by reduced vessel density and increased apoptosis. Neuroinflammation also occurred as large numbers of microglia, along with inflammatory cytokines, were found at sites of A?? accumulation.
The authors conclude that early-onset A?? accumulation occurs predominantly in the cerebral microvasculature and appears largely responsible for the neuroinflammation in these mice. They also demonstrate the utility of Tg-SwDI mice in studying cerebral amyloid angiopathies, such as Alzheimer's disease.
The second article, by Kumar-Singh et al., "Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls," utilizes two different transgenic mice: Tg2576 and PSAPP. Both models produce dense-core plaques, highly concentrated deposits of A??, and were used to investigate the possible association of blood vessels with A?? deposits.
In these mice, dense-core plaques associated with cerebral vessels with high specificity. There was also evidence of vessel damage and blood-brain barrier damage, resulting in release of A?? through the vessel walls and accumulation of plaques next to the vessels. These data confirm previous observations in humans that senile plaques associate with blood vessels, especially in the vasculotropic Flemish type of Alzheimer's disease.
The authors propose a model of dense-core plaque formation that is dependent on cerebral vessels. As A?? is cleared from the brain, it exerts a cytotoxic effect on the endothelial cells of the vascular wall (a process that may be exacerbated if clearance is impaired). This leads to loss of vessel integrity and accumulation of A?? in the area surrounding the compromised vessel wall. Eventually, the damage is so great that the blood vessel deteriorates beyond functional use and new vessels form to pick up the slack. The result is a multicentric dense-core plaque that associates with multiple vessels.
These studies describe several animal models for further examining the pathogenesis and treatment of Alzheimer's disease and related cerebral amyloid angiopathies. And both studies confirm that A?? generated by neurons accumulates in blood vessels following attempted clearance of excess A?? peptides. Thus, study of novel therapies that reduce the blood vessel-associated deposition of A?? may prove beneficial to patients with Alzheimer's disease.
*Miao J, Xu F, Davis J, Otte-H?ller I, Verbeek MM, Van Nostrand WE: Cerebral microvascular A?? deposition induces vascular degeneration and neuroinflammation in transgenic mice expressing human vasculotropic mutant A??PP. Am J Pathol 2005, 167: 505-515
†Kumar-Singh S, Pirici D, McGowan E, Serneels S, Ceuterick C, Hardy J, Duff K, Dickson D, Van Broeckhoven C: Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls. Am J Pathol 2005, 167: 527-543
*Work was performed at Stony Brook University, New York. †Work was performed at the Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Belgium.
For press copies of the article, please contact Audra Cox at 301-634-7409.
The American Journal of Pathology, the official journal of the American Society for Investigative Pathology (ASIP), seeks to publish high-quality original papers on the cellular and molecular mechanisms of disease. The editors accept manuscripts which report important findings on disease pathogenesis or basic biological mechanisms that relate to disease, without preference for a specific method of analysis. High priority is given to studies on human disease and relevant experimental models using cellular, molecular, biological, animal, chemical and immunological approaches in conjunction with morphology.
Audra Cox
acoxasip
301-634-7409
American Journal of Pathology
ajp.amjpathol
четверг, 7 июля 2011 г.
Exercise variety - not intensity - appears to reduce some Alzheimer's disease risk
The variety of leisure and physical activity one engages in -- and not its intensity in terms of calories expended - may
reduce dementia risk in older people, according to researchers at Johns Hopkins. An association between variety of activity
and dementia risk, however, did not hold up in those with the so-called APOE-4 genetic predisposition to the disease found in
about one-quarter to one-third of Alzheimer's patients, according to a report appearing in the April 1, 2005, issue of the
American Journal of Epidemiology.
General physical activity is already known to enhance cardiovascular health and help maintain independence and quality of
life in older people, but the results of this study - which establish a statistical association, and not a direct cause and
effect, between variety of exercise and reduced dementia risk -- suggest that participating in a number of different
activities may be as or more important than frequency, duration, and intensity of physical activity with respect to dementia
risk, according to the report.
"We don't yet know why this association exists or what causes it. It could well be that maintaining a variety of activities
keeps more parts of the brain active, or that this variety reflects better engagement in both physical and social activities.
Confirmation of this association in future studies may provide an additional impetus for people to remain or become engaged
in several physical and other leisure activities later in life," says Constantine G. Lyketsos, M.D., professor of psychiatry
and behavioral sciences at Johns Hopkins and senior author on the report.
The study included 3,375 men and women age 65 years or older who participated in the Cardiovascular Health Cognition Study
from 1992 to 2000 and who did not have dementia at the onset of the study. Each study volunteer was asked to fill out a
questionnaire about the frequency and duration of the 15 most common types of physical activity in older adults, including
walking, household chores, mowing, raking, gardening, hiking, jogging, biking, exercise cycling, dancing, aerobics, bowling,
golfing, general exercise and swimming. The researchers then created an activity index, calculated as the number of different
activities each subject participated in over the previous two weeks. Other measurements, including APOE gentotype, age,
gender, education level, ethnicity, smoking, alcohol use, and other physical and mental health-related history, were also
considered in the study.
The researchers found 480 new cases of dementia over an average of 5.4 years of follow-up. Among these, dementia occurred
less frequently in those participating in more activities relative to those who participated in fewer activities (one or no
activity had 130 cases, two activities had 152 cases, three activities had 113 cases, four or more activities had 84 cases).
The association held true for all types of dementia, including Alzheimer's disease and vascular dementia. The association did
not hold true for those who have the APOE-4 genotype.
"These findings, taken together with recent findings from our colleagues at the University of Chicago studying physical
activity and plaque buildup in the brains of mice with Alzheimer's (published this year in the journal Cell) provide a good
picture from basic and clinical science of how activity and exercise work to reduce the risk of dementia," says Lyketsos.
According to the Alzheimer's Association, dementia is a group of diseases that all gradually destroy brain cells and lead to
progressive decline in mental function. An estimated 4.5 million Americans have Alzheimer's disease, the most common form of
dementia. The number of American's with Alzheimer's disease has more than doubled since 1980 and is projected to reach 11.3
to 16 million by the year 2050.
Other authors of the report are Laura Jean Podewils, Eliseo Gualler, Linda Fried and Michelle Carson of Johns Hopkins, and
Lewis H. Kuller and Oscar L. Lopez of the University of Pittsburg. The research was funded by the National Heart, Lung and
Blood Institute and the National Institute on Aging.
On the Web:
hopkinsmedicine/Psychiatry/Clinical/geriatric.html
aje.oupjournals
Contact: Trent Stockton
tstockt1jhmi
410-955-8665
Johns Hopkins Medical Institutions
hopkinsmedicine
reduce dementia risk in older people, according to researchers at Johns Hopkins. An association between variety of activity
and dementia risk, however, did not hold up in those with the so-called APOE-4 genetic predisposition to the disease found in
about one-quarter to one-third of Alzheimer's patients, according to a report appearing in the April 1, 2005, issue of the
American Journal of Epidemiology.
General physical activity is already known to enhance cardiovascular health and help maintain independence and quality of
life in older people, but the results of this study - which establish a statistical association, and not a direct cause and
effect, between variety of exercise and reduced dementia risk -- suggest that participating in a number of different
activities may be as or more important than frequency, duration, and intensity of physical activity with respect to dementia
risk, according to the report.
"We don't yet know why this association exists or what causes it. It could well be that maintaining a variety of activities
keeps more parts of the brain active, or that this variety reflects better engagement in both physical and social activities.
Confirmation of this association in future studies may provide an additional impetus for people to remain or become engaged
in several physical and other leisure activities later in life," says Constantine G. Lyketsos, M.D., professor of psychiatry
and behavioral sciences at Johns Hopkins and senior author on the report.
The study included 3,375 men and women age 65 years or older who participated in the Cardiovascular Health Cognition Study
from 1992 to 2000 and who did not have dementia at the onset of the study. Each study volunteer was asked to fill out a
questionnaire about the frequency and duration of the 15 most common types of physical activity in older adults, including
walking, household chores, mowing, raking, gardening, hiking, jogging, biking, exercise cycling, dancing, aerobics, bowling,
golfing, general exercise and swimming. The researchers then created an activity index, calculated as the number of different
activities each subject participated in over the previous two weeks. Other measurements, including APOE gentotype, age,
gender, education level, ethnicity, smoking, alcohol use, and other physical and mental health-related history, were also
considered in the study.
The researchers found 480 new cases of dementia over an average of 5.4 years of follow-up. Among these, dementia occurred
less frequently in those participating in more activities relative to those who participated in fewer activities (one or no
activity had 130 cases, two activities had 152 cases, three activities had 113 cases, four or more activities had 84 cases).
The association held true for all types of dementia, including Alzheimer's disease and vascular dementia. The association did
not hold true for those who have the APOE-4 genotype.
"These findings, taken together with recent findings from our colleagues at the University of Chicago studying physical
activity and plaque buildup in the brains of mice with Alzheimer's (published this year in the journal Cell) provide a good
picture from basic and clinical science of how activity and exercise work to reduce the risk of dementia," says Lyketsos.
According to the Alzheimer's Association, dementia is a group of diseases that all gradually destroy brain cells and lead to
progressive decline in mental function. An estimated 4.5 million Americans have Alzheimer's disease, the most common form of
dementia. The number of American's with Alzheimer's disease has more than doubled since 1980 and is projected to reach 11.3
to 16 million by the year 2050.
Other authors of the report are Laura Jean Podewils, Eliseo Gualler, Linda Fried and Michelle Carson of Johns Hopkins, and
Lewis H. Kuller and Oscar L. Lopez of the University of Pittsburg. The research was funded by the National Heart, Lung and
Blood Institute and the National Institute on Aging.
On the Web:
hopkinsmedicine/Psychiatry/Clinical/geriatric.html
aje.oupjournals
Contact: Trent Stockton
tstockt1jhmi
410-955-8665
Johns Hopkins Medical Institutions
hopkinsmedicine
понедельник, 4 июля 2011 г.
Conference To Share Cutting Edge Developments In Dementia Research
With more than 35 million people worldwide living with Alzheimer's disease or a related dementia, the search for answers has never been more critical.
With this in mind, the very best minds in dementia research and care, both in Canada and abroad, will converge on Toronto today at the 5th Canadian Conference on Dementia to share the very latest developments in the field.
"Dementia is a rapidly growing issue for Canadians, an issue that needs immediate attention if we are to mitigate the impact of this illness on our health and social systems," says Dr. Ron Keren, Conference Chair. "The Canadian Conference on Dementia is an opportunity for the international community of experts to come together and share critical information on the latest in research and care."
The conference will open with two keynote presentations by Dr. Margaret Lock (McGill University) and Dr. Mary Ganguli (University of Pittsburgh), followed by the presentation of I'm Still Here, a powerful research-based play illustrating the perspective of persons living with dementia and their family partners in care.
The conference will also feature sessions on risk factors, diagnosis, treatments, quality of life, caregiving and the need for a national dementia strategy. This diverse program will explore the challenges of dementia, address the issues facing people with the illness, and present ways to help change the future of the disease.
The Canadian Conference on Dementia will take place October 1 to 3 at the Westin Harbor Castle Hotel in Toronto. To see the full schedule of speakers and topics, please visit ccd2009.ca.
Canadian Conference on Dementia
The Canadian Conference on Dementia is a biannual national conference on dementia that is sponsored by the Canadian Geriatrics Society, the Canadian Academy of Geriatric Psychiatry, the Canadian Neurological Society, the Consortium of Canadian Centres for Clinical Cognitive Research, the Canadian Institutes of Health Research-Institute of Aging, the Canadian Dementia Knowledge Translation Network and the Alzheimer Society of Canada.
Source
Alzheimer's Society
With this in mind, the very best minds in dementia research and care, both in Canada and abroad, will converge on Toronto today at the 5th Canadian Conference on Dementia to share the very latest developments in the field.
"Dementia is a rapidly growing issue for Canadians, an issue that needs immediate attention if we are to mitigate the impact of this illness on our health and social systems," says Dr. Ron Keren, Conference Chair. "The Canadian Conference on Dementia is an opportunity for the international community of experts to come together and share critical information on the latest in research and care."
The conference will open with two keynote presentations by Dr. Margaret Lock (McGill University) and Dr. Mary Ganguli (University of Pittsburgh), followed by the presentation of I'm Still Here, a powerful research-based play illustrating the perspective of persons living with dementia and their family partners in care.
The conference will also feature sessions on risk factors, diagnosis, treatments, quality of life, caregiving and the need for a national dementia strategy. This diverse program will explore the challenges of dementia, address the issues facing people with the illness, and present ways to help change the future of the disease.
The Canadian Conference on Dementia will take place October 1 to 3 at the Westin Harbor Castle Hotel in Toronto. To see the full schedule of speakers and topics, please visit ccd2009.ca.
Canadian Conference on Dementia
The Canadian Conference on Dementia is a biannual national conference on dementia that is sponsored by the Canadian Geriatrics Society, the Canadian Academy of Geriatric Psychiatry, the Canadian Neurological Society, the Consortium of Canadian Centres for Clinical Cognitive Research, the Canadian Institutes of Health Research-Institute of Aging, the Canadian Dementia Knowledge Translation Network and the Alzheimer Society of Canada.
Source
Alzheimer's Society
пятница, 1 июля 2011 г.
New Survey Shows Confronting Alzheimer's Disease A Key Issue In 2008 Presidential Election
With less than a month until the presidential caucus and primary season officially begins, a poll released by the Alzheimer's Association indicates how the Presidential candidates plan to address the escalating Alzheimer epidemic could determine who Americans vote for in November. Finding a way to halt or delay the progression of Alzheimer's disease is paramount on the minds of Americans. In a new national survey conducted by Hart Research, more than two out of three Americans polled (68 percent) think it is important to increase the amount of Alzheimer disease research funding and two out of three voters (67 percent) would be more likely to select a Presidential candidate who supports increased government funding for Alzheimer research.
"Every Presidential candidate needs to understand that Alzheimer's is an important issue for American voters," said Harry Johns, President and CEO of the Alzheimer's Association. "This disease steals millions of lives and threatens to overwhelm our healthcare and long term care systems. The American people understand that more must be done to stop this escalating epidemic and they want a President who will act to address the concerns of the millions affected by Alzheimer's today and those who will face it tomorrow."
Alzheimer's Disease Feared More Than Natural Disasters
- The survey revealed that Americans are more afraid of developing Alzheimer's disease (69 percent) than becoming a victim of a natural disaster, such as a wildfire or hurricane (42 percent).
- Somewhat surprisingly, age does not play a factor here as 18-34 year olds (65 percent) are just as likely as seniors (64 percent) to be concerned about themselves or a family member developing Alzheimer's.
Alzheimer's is a Bipartisan Issue
- Today there are as many 5 million Americans living with Alzheimer's disease and that number is expected to grow to as many as 16 million by 2050. Among voters polled the concern about developing Alzheimer's cuts across party lines with Republicans (64 percent), Democrats (68 percent), and Independents (66 percent).
An Overwhelming Financial Burden to Families and Health Care System
- Alzheimer's disease is intrinsically linked to long-term care because many of those with the disease are ultimately placed in long term care facilities when families can no longer provide the round-the-clock care people in the advanced stages of the disease require. Millions of families rely on Medicaid to cover long term care costs due to the fact that caring for someone with Alzheimer's can quickly deplete family assets.
- This survey found financing the expensive costs of long term care was a key issue on voters' minds, as almost two thirds (62 percent) polled indicated they would be more likely to vote for a Presidential candidate who sought to increase financial assistance for families taking care of a loved one with Alzheimer's. Further, almost three out of four (70 percent) said reforming Medicare and Medicaid to provide better care for the growing Alzheimer disease population could be a determining factor in who they would choose as the next president.
Women are more likely to vote for candidate who addresses Alzheimer issues
- Women are more likely to vote for a candidate who supports increasing government funding for Alzheimer's research (72 percent vs. 63 percent of men); women are more likely to choose a candidate who supports Medicare and Medicaid reforms to help those living with Alzheimer's receive better care (77 percent vs. 66 percent of men); and they are more likely to vote for candidates who support increased financial assistance for persons with Alzheimer's to receive long term care (69 percent vs. 59 percent of men.)
The Alzheimer's Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's. For more information, visit alz.
The Alzheimer's Association Survey
The Alzheimer's Association poll, conducted by Peter D. Hart Research Associates, Inc., was created to measure the impact of how Alzheimer issues would impact voters. The nationwide survey was conducted via telephone with a random sample of 801 adults. The overall sampling error for this survey is +/- 3.5%.
Alzheimer's Association
"Every Presidential candidate needs to understand that Alzheimer's is an important issue for American voters," said Harry Johns, President and CEO of the Alzheimer's Association. "This disease steals millions of lives and threatens to overwhelm our healthcare and long term care systems. The American people understand that more must be done to stop this escalating epidemic and they want a President who will act to address the concerns of the millions affected by Alzheimer's today and those who will face it tomorrow."
Alzheimer's Disease Feared More Than Natural Disasters
- The survey revealed that Americans are more afraid of developing Alzheimer's disease (69 percent) than becoming a victim of a natural disaster, such as a wildfire or hurricane (42 percent).
- Somewhat surprisingly, age does not play a factor here as 18-34 year olds (65 percent) are just as likely as seniors (64 percent) to be concerned about themselves or a family member developing Alzheimer's.
Alzheimer's is a Bipartisan Issue
- Today there are as many 5 million Americans living with Alzheimer's disease and that number is expected to grow to as many as 16 million by 2050. Among voters polled the concern about developing Alzheimer's cuts across party lines with Republicans (64 percent), Democrats (68 percent), and Independents (66 percent).
An Overwhelming Financial Burden to Families and Health Care System
- Alzheimer's disease is intrinsically linked to long-term care because many of those with the disease are ultimately placed in long term care facilities when families can no longer provide the round-the-clock care people in the advanced stages of the disease require. Millions of families rely on Medicaid to cover long term care costs due to the fact that caring for someone with Alzheimer's can quickly deplete family assets.
- This survey found financing the expensive costs of long term care was a key issue on voters' minds, as almost two thirds (62 percent) polled indicated they would be more likely to vote for a Presidential candidate who sought to increase financial assistance for families taking care of a loved one with Alzheimer's. Further, almost three out of four (70 percent) said reforming Medicare and Medicaid to provide better care for the growing Alzheimer disease population could be a determining factor in who they would choose as the next president.
Women are more likely to vote for candidate who addresses Alzheimer issues
- Women are more likely to vote for a candidate who supports increasing government funding for Alzheimer's research (72 percent vs. 63 percent of men); women are more likely to choose a candidate who supports Medicare and Medicaid reforms to help those living with Alzheimer's receive better care (77 percent vs. 66 percent of men); and they are more likely to vote for candidates who support increased financial assistance for persons with Alzheimer's to receive long term care (69 percent vs. 59 percent of men.)
The Alzheimer's Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's. For more information, visit alz.
The Alzheimer's Association Survey
The Alzheimer's Association poll, conducted by Peter D. Hart Research Associates, Inc., was created to measure the impact of how Alzheimer issues would impact voters. The nationwide survey was conducted via telephone with a random sample of 801 adults. The overall sampling error for this survey is +/- 3.5%.
Alzheimer's Association
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