NICE Recommendation On Alzheimer's Medicines
Amyloid
Tuesday, January 31, 2006
The Association of the British Pharmaceutical Industry (ABPI) today welcomed the revised position on Alzheimer's medicines expressed by NICE while expressing disappointment that their value for people with mild Alzheimer's has still not been recognised. And the ABPI also stressed that it was important that NICE's recommendation actually resulted in people receiving the medicines and not still being subject to the vagaries of local funding. “There is no point in NICE making recommendations that are then ignored on the ground,” said Dr Richard Barker, Director General of the ABPI. “We want people to benefit from these medicines yet, sadly, it is often the case that local health authorities put budgetary considerations over people's wellbeing by not allowing them to be prescribed.” Although the current Alzheimer's treatments are licensed for use in mild to moderate Alzheimer's - as is the case throughout Europe and around the world - the NICE recommendation is for use with those who have moderate Alzheimer's only. “While the decision to allow patients with moderate Alzheimer's treatment with these medicines is naturally welcome, it is disappointing that their potential value in those with the mild form of the condition has not been recognised,” Dr Barker said. “Doing everything possible to prevent or at least slow down the development of this distressing condition should be a top priority for the health service.”
Monday, January 30, 2006
Walking and dementia in physically capable elderly men.
Abbott RD, White LR, Ross GW, Masaki KH, Curb JD, Petrovitch H
CONTEXT: Evidence suggests that physical activity may be related to the clinical expression of dementia. Whether the association includes low-intensity activity such as walking is not known.
CONTEXT: Evidence suggests that physical activity may be related to the clinical expression of dementia. Whether the association includes low-intensity activity such as walking is not known.
OBJECTIVE: To examine the association between walking and future risk of dementia in older men. DESIGN: Prospective cohort study.
ETTING AND PARTICIPANTS: Distance walked per day was assessed from 1991 to 1993 in 2257 physically capable men aged 71 to 93 years in the Honolulu-Asia Aging Study. Follow-up for incident dementia was based on neurological assessment at 2 repeat examinations (1994-1996 and 1997-1999).
MAIN OUTCOME MEASURES: Overall dementia, Alzheimer disease, and vascular dementia. RESULTS: During the course of follow-up, 158 cases of dementia were identified (15.6/1000 person-years). After adjusting for age, men who walked the least (<0.25>2 mile/d), an excess risk of dementia was also observed in those who walked 0.25 to 1 mile/d (17.6 vs 10.3/1000 person-years; RH, 1.71; 95% CI, 1.02-2.86). These associations persisted after accounting for other factors, including the possibility that limited amounts of walking could be the result of a decline in physical function due to preclinical dementia.
CONCLUSIONS: Findings suggest that walking is associated with a reduced risk of dementia. Promoting active lifestyles in physically capable men could help late-life cognitive function.
National Library of Medicine (NLM) http://www.nlm.nih.gov/
The effect of planned walking on communication in Alzheimer's disease.Read on
Sunday, January 29, 2006
Sound Body, Mind: Scientific study showing direct link between exercise and brain function
Carl Cotman of UC Irvine conducts experiments on mice that relate exercise to the onset of Alzheimer's disease.
A faster mile, bigger biceps, more stamina - all are proof that exercise hones the body. Less tangible, but no less important, is the effect on the mind.
Over the last decade, neuroscientists have been churning out an abundance of data pointing to changes in the brain after physical activity. Some researchers have even suggested that the type of exercise matters - as does the age at which it begins.
"I would absolutely recommend people exercise for the mental benefits - especially the elderly," says Henriette van Praag, a staff scientist at the Salk Institute for Biological Studies in San Diego. "People don't care about whether they're a size 4 or a size 6 as they get older. But they do care where their car keys are and whether they'll have the ability to play their card games and enjoy life."
http://ura-inform.com/archive/?/2006/01/27/~/57986
Saturday, January 28, 2006
Targeted nanoparticles for drug delivery through the blood-brain barrier for Alzheimer's disease.
Alzheimer's disease (AD) is the most common cause of dementia among the elderly, affecting 5% of Americans over age 65, and 20% over age 80. An excess of senile plaques (beta-amyloid protein) and neurofibrillary tangles (tau protein), ventricular enlargement, and cortical atrophy characterizes it. Unfortunately, targeted drug delivery to the central nervous system (CNS), for the therapeutic advancement of neurodegenerative disorders such as Alzheimer's, is complicated by restrictive mechanisms imposed at the blood-brain barrier (BBB). Opsonization by plasma proteins in the systemic circulation is an additional impediment to cerebral drug delivery. This review gives an account of the BBB and discusses the literature on biodegradable polymeric nanoparticles (NPs) with appropriate surface modifications that can deliver drugs of interest beyond the BBB for diagnostic and therapeutic applications in neurological disorders, such as AD. The physicochemical properties of the NPs at different surfactant concentrations, stabilizers, and amyloid-affinity agents could influence the transport mechanism.
Clioquinol for the treatment of Alzheimer's Disease.Read on
Alzheimer's disease: stage-related interventions.Read on
Cholesterol and apoe: a target for Alzheimer's disease therapeutics.Read on
Friday, January 27, 2006
Three New Studies Aimed at Alzheimer's Caregivers
Caring for a loved one with Alzheimer's disease? You may be eligible to participate in one of three new studies currently recruiting patients at New York University (NYU) School of Medicine. All are aimed at showing whether short-term counseling can ease the psychological stress and depression of those with Alzheimer's and their family members. “Alzheimer's disease is a tragedy not only to its victims, but also to their caregivers,” says Mary Mittelman, Dr.P.H., Director of the Psychosocial Research and Support Program at the NYU School of Medicine's Silberstein Institute. “Primary caregivers often experience stress, depression, and other emotional problems as a result of the continuing and demanding levels of care required by people with Alzheimer's, the most common form of dementia affecting people over 65.”These studies were inspired by the success of a previous trial at the NYU School of Medicine that showed that even a short period of counseling can have a long-term beneficial impact on the emotional well-being of people taking care of spouses with Alzheimer's disease. Dr. Mittelman and her colleagues found that this unique counseling and support program substantially eases the depression of spouse caregivers of Alzheimer's patients. The benefits persisted even three years after counseling ended. Even when spouse caregivers have supportive networks, there can still be communication difficulties within families that require counseling to resolve.
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Treatment Of Down Syndrome In Mice Restores Nerve Growth In Cerebellummore...
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Thursday, January 26, 2006
MorphoSys says Roche to start Phase I trial with antibody to treat Alzheimers
MUNICH (AFX) - MorphoSys AG said Roche Holding AG has filed all necessary applications to start a European Phase I clinical trial with its antibody to treat Alzheimers disease, triggering a clinical milestone payment from Roche to the Munich-based company. No further financial details were disclosed. The antibody is from MorphoSys' HuCAL antibody library. It targets abnormal build-ups of amyloid beta protein in cerebral tissue, which are typical of Alzheimer's patients, and is intended to help remove them. MorphoSys said the antibody has shown -- in pre-clinical tests -- a high affinity of binding to amyloid beta plaques and was able to bind specifically to amyloid plaques in human brain tissue samples taken from Alzheimers patients. The antibody was further tested in an animal model of Alzheimers disease and was shown to cross the blood-brain-barrier and to bind to amyloid beta plaques within the brain. It added that international research on Alzheimers sees the breakdown of amyloid beta formations as a promising starting point towards treatment and that removal of the accumulations has been linked to an increase in correct cognitive functioning.
http://www.medicalnewstoday.com/medicalnews.php?newsid=36596
Fighting Alzheimer's Disease: Go for the Beta-Amyloid!
Brain Cell Activity Increases Amyloid Beta: From MedicineWorld.Org
Beta-amyloid: Alzheimer's disease and brain beta-amyloidoses.
MUNICH (AFX) - MorphoSys AG said Roche Holding AG has filed all necessary applications to start a European Phase I clinical trial with its antibody to treat Alzheimers disease, triggering a clinical milestone payment from Roche to the Munich-based company. No further financial details were disclosed. The antibody is from MorphoSys' HuCAL antibody library. It targets abnormal build-ups of amyloid beta protein in cerebral tissue, which are typical of Alzheimer's patients, and is intended to help remove them. MorphoSys said the antibody has shown -- in pre-clinical tests -- a high affinity of binding to amyloid beta plaques and was able to bind specifically to amyloid plaques in human brain tissue samples taken from Alzheimers patients. The antibody was further tested in an animal model of Alzheimers disease and was shown to cross the blood-brain-barrier and to bind to amyloid beta plaques within the brain. It added that international research on Alzheimers sees the breakdown of amyloid beta formations as a promising starting point towards treatment and that removal of the accumulations has been linked to an increase in correct cognitive functioning.
http://www.medicalnewstoday.com/medicalnews.php?newsid=36596
Fighting Alzheimer's Disease: Go for the Beta-Amyloid!
Brain Cell Activity Increases Amyloid Beta: From MedicineWorld.Org
Beta-amyloid: Alzheimer's disease and brain beta-amyloidoses.
Wednesday, January 25, 2006
What You Need To Know Now
By Dr. Isadore Rosenfeld
Young women are apt to worry about developing cancer of the breast (although more of them die from lung cancer), and heart attacks and stroke are the greatest concern of adult males. But Alzheimer’s disease (AD) is everyone’s greatest fear as we grow older. Alzheimer’s currently affects 4.5 million Americans; one in 10 of us has at least one family member suffering from it. That’s considerably more than in 1980—and the numbers are growing. Within the next 50 years, as many as 16 million men and women in the U.S. are expected to develop it. Alzheimer’s is named after the German doctor Alois Alzheimer, who in 1906 described a form of “cognitive impairment” that he considered to be a disorder of mid-life. He believed, as some still do, that the memory and behavioral changes—what we now call Alzheimer’s—in older people are part and parcel of the aging process.We now know that Alzheimer’s is a disease, regardless of the age at which it appears. Although it most often accompanies the aging process, growing older does not cause this disease. In fact, the vast majority of seniors do not have it. Those with “senile dementia” do not necessarily have AD. Their abnormal behavior may be due to any one of several neurological disorders to which older people are vulnerable.The brain of someone who died with AD contains two abnormal structures characteristic of the disease: plaques and tangles. Plaques are clumps of beta amyloid protein that accumulate around the brain’s nerve cells and eventually cause them to die. Tangles are twisted strands of another protein (called “tau”) that form within the cells. Many scientists believe that one or both of these proteins, more likely the beta amyloid, cause AD; they are now seeking ways to prevent them from occurring in the brain. An experimental “vaccine” has been developed that seems to be able to do so in animals. If it is found to work safely in humans, it could, conceivably, help control this terrible disease. The most recent speculation about the cause of Alzheimer’s implicates insulin. Researchers at Rhode Island Hospital and Brown University Medical School have found that insulin concentrations in the brain drop dramatically in early Alzheimer’s and continue to fall as the disease progresses. They opine that this may contribute to the cell death and tangles characteristic of AD. Another hallmark of Alzheimer’s—low levels of a substance called acetylcholine—also is directly linked to loss of insulin, all of which suggests that Alzheimer’s may be a form of diabetes. This opens up promising new possibilities in solving the enigma of Alzheimer’s disease.Is Alzheimer’s hereditary? There are two types of AD: familial and sporadic. The former affects less than 10% of patients, usually has its onset before age 65 and is accompanied by gene mutations on three chromosomes. In the more common sporadic (late-onset) form of AD, one gene may be involved. While there is no obvious inheritance pattern, if a parent or sibling has AD, you are at greater risk yourself. A downward spiral. Alzheimer’s typically begins with memory loss, especially of recent events. Patients can usually remember an event that occurred 50 years ago but may not recall what they ate for breakfast that morning. The disease progresses at an unpredictable rate. In addition to memory loss, there is often intellectual impairment, confusion and, in the late stages, inability to look after oneself. All this is frequently accompanied by personality changes and even violent behavior. Once the diagnosis of Alzheimer’s is made, average survival is about eight years but can be as long as 20.Late-stage AD is often devastating to family members. Many feel frustrated, worried and guilty—especially when a loved one must leave home to receive the kind of care that can best be given in a nursing home or other facility. The diagnosis: Rule out other possibilities. There is no single test that specifically confirms the presence of Alzheimer’s. But a proper history and available diagnostic procedures can identify it in 90% of cases. Do not accept this diagnosis, however, before making sure that the following conditions have been considered:
• Nutritional deficiencies (especially of the B vitamins). Patients diagnosed with Alzheimer’s are often miraculously “cured” when they eat a balanced diet.
• Medication. Tranquilizers, anti-anxiety drugs and other mood-altering agents can affect behavior.
• Multiple small strokes (usually due to poorly controlled high blood pressure). If unrecognized and untreated, they can damage the brain and cause behavioral changes.
• Depression for any reason—loneliness, bereavement, social adversities. It can lead to withdrawal and be mistaken for AD.
• Low thyroid function. This may cause the impaired cognition and lack of interest attributed to Alzheimer’s in older people. The behavior disappears when the missing thyroid hormone is replaced.
• Other diseases of the brain that can be accompanied by symptoms of AD. These include brain tumors, multiple sclerosis, Lou Gehrig’s disease and Parkinson’s.
• A blow to the head. It can cause blood to accumulate under the skull, press on the brain and result in behavioral changes.
• Lyme disease. An infection that strikes many different organs, it also can affect the brain.
So, before concluding that anyone has Alzheimer’s, make sure that all of these conditions have been ruled out. Until there’s a cure... There currently is no cure for Alzheimer’s, but there are several drugs that may improve or stabilize mild symptoms. Those approved by the FDA include Cognex, Aricept, Exelon, Razadyne and, in advanced cases, Namenda. Frankly, these are only stopgap measures until a cure is found. However, given the intensive current research in this area, I believe there is reason for optimism.
Please add info@eversave.com to your address book to continue receiving great savings from Healthier, see how.
Axonyx Completes First Phase I Trial with Posiphen for Alzheimer's ...
What You Need To Know Now
By Dr. Isadore Rosenfeld
Young women are apt to worry about developing cancer of the breast (although more of them die from lung cancer), and heart attacks and stroke are the greatest concern of adult males. But Alzheimer’s disease (AD) is everyone’s greatest fear as we grow older. Alzheimer’s currently affects 4.5 million Americans; one in 10 of us has at least one family member suffering from it. That’s considerably more than in 1980—and the numbers are growing. Within the next 50 years, as many as 16 million men and women in the U.S. are expected to develop it. Alzheimer’s is named after the German doctor Alois Alzheimer, who in 1906 described a form of “cognitive impairment” that he considered to be a disorder of mid-life. He believed, as some still do, that the memory and behavioral changes—what we now call Alzheimer’s—in older people are part and parcel of the aging process.We now know that Alzheimer’s is a disease, regardless of the age at which it appears. Although it most often accompanies the aging process, growing older does not cause this disease. In fact, the vast majority of seniors do not have it. Those with “senile dementia” do not necessarily have AD. Their abnormal behavior may be due to any one of several neurological disorders to which older people are vulnerable.The brain of someone who died with AD contains two abnormal structures characteristic of the disease: plaques and tangles. Plaques are clumps of beta amyloid protein that accumulate around the brain’s nerve cells and eventually cause them to die. Tangles are twisted strands of another protein (called “tau”) that form within the cells. Many scientists believe that one or both of these proteins, more likely the beta amyloid, cause AD; they are now seeking ways to prevent them from occurring in the brain. An experimental “vaccine” has been developed that seems to be able to do so in animals. If it is found to work safely in humans, it could, conceivably, help control this terrible disease. The most recent speculation about the cause of Alzheimer’s implicates insulin. Researchers at Rhode Island Hospital and Brown University Medical School have found that insulin concentrations in the brain drop dramatically in early Alzheimer’s and continue to fall as the disease progresses. They opine that this may contribute to the cell death and tangles characteristic of AD. Another hallmark of Alzheimer’s—low levels of a substance called acetylcholine—also is directly linked to loss of insulin, all of which suggests that Alzheimer’s may be a form of diabetes. This opens up promising new possibilities in solving the enigma of Alzheimer’s disease.Is Alzheimer’s hereditary? There are two types of AD: familial and sporadic. The former affects less than 10% of patients, usually has its onset before age 65 and is accompanied by gene mutations on three chromosomes. In the more common sporadic (late-onset) form of AD, one gene may be involved. While there is no obvious inheritance pattern, if a parent or sibling has AD, you are at greater risk yourself. A downward spiral. Alzheimer’s typically begins with memory loss, especially of recent events. Patients can usually remember an event that occurred 50 years ago but may not recall what they ate for breakfast that morning. The disease progresses at an unpredictable rate. In addition to memory loss, there is often intellectual impairment, confusion and, in the late stages, inability to look after oneself. All this is frequently accompanied by personality changes and even violent behavior. Once the diagnosis of Alzheimer’s is made, average survival is about eight years but can be as long as 20.Late-stage AD is often devastating to family members. Many feel frustrated, worried and guilty—especially when a loved one must leave home to receive the kind of care that can best be given in a nursing home or other facility. The diagnosis: Rule out other possibilities. There is no single test that specifically confirms the presence of Alzheimer’s. But a proper history and available diagnostic procedures can identify it in 90% of cases. Do not accept this diagnosis, however, before making sure that the following conditions have been considered:
• Nutritional deficiencies (especially of the B vitamins). Patients diagnosed with Alzheimer’s are often miraculously “cured” when they eat a balanced diet.
• Medication. Tranquilizers, anti-anxiety drugs and other mood-altering agents can affect behavior.
• Multiple small strokes (usually due to poorly controlled high blood pressure). If unrecognized and untreated, they can damage the brain and cause behavioral changes.
• Depression for any reason—loneliness, bereavement, social adversities. It can lead to withdrawal and be mistaken for AD.
• Low thyroid function. This may cause the impaired cognition and lack of interest attributed to Alzheimer’s in older people. The behavior disappears when the missing thyroid hormone is replaced.
• Other diseases of the brain that can be accompanied by symptoms of AD. These include brain tumors, multiple sclerosis, Lou Gehrig’s disease and Parkinson’s.
• A blow to the head. It can cause blood to accumulate under the skull, press on the brain and result in behavioral changes.
• Lyme disease. An infection that strikes many different organs, it also can affect the brain.
So, before concluding that anyone has Alzheimer’s, make sure that all of these conditions have been ruled out. Until there’s a cure... There currently is no cure for Alzheimer’s, but there are several drugs that may improve or stabilize mild symptoms. Those approved by the FDA include Cognex, Aricept, Exelon, Razadyne and, in advanced cases, Namenda. Frankly, these are only stopgap measures until a cure is found. However, given the intensive current research in this area, I believe there is reason for optimism.
Please add info@eversave.com to your address book to continue receiving great savings from Healthier, see how.
Axonyx Completes First Phase I Trial with Posiphen for Alzheimer's ...
Tuesday, January 24, 2006
Blackcurrants May Protect Brain
British blackcurrants may hold the key to preventing Alzheimer’s disease, researchers have reported. Researchers in New Zealand say the blackcurrant - which grows freely in British gardens - is rich in compounds which appear to protect against the brain disease. The researchers said two compounds anthocyanins and polyphenolics are found in two fruits, the blackcurrant and the boysenberry in the USA. The laboratory studies of brain cells suggest they have a powerful ability to protect against damage caused by amyloid-beta and dopamine, chemicals involved with Alzheimer’s disease. But the British blackberry has been bred to be a dark berry - and contains greater quantities of anthocyanin than the boysenberry. Details of the research by Dilip Ghosh, of the Horticulture and Food Research Institute, New Zealand. James Joseph, of Tufts University, said : "We have evidence that the compounds protect against Alzheimer’s by influencing the early gene expression in learning and memory, which influences cell signaling pathways that help neuronal cells communicate with each other."
http://www.medicalnewstoday.com/medicalnews.php?newsid=36488
http://www.medicalnewstoday.com/medicalnews.php?newsid=36488
Monday, January 23, 2006
New Compound Stops Brain Cell Degeneration In Alzheimer's Disease
Drug discovery researchers at Northwestern University have developed a novel orally administered compound specifically targeted to suppress brain cell inflammation and neuron loss associated with Alzheimer's disease. The compound is also rapidly absorbed by the brain and is non-toxic - important considerations for a central nervous system drug that might need to be taken for extended periods. http://www.medicalnewstoday.com/medicalnews.php?newsid=36434
Sunday, January 22, 2006
Emotional response to social dancing and walks in persons with dementia
The emotional response to social dancing and walks in persons with dementia was studied to better understand the feasibility, popularity, and meaning of these activities from the perspective of the patient. Social dance events and walks were videotaped and analyzed using Husserl's philosophy as a basis for the analysis. Six persons with dementia participated in the study. The results are described in terms of four interrelated themes: 1) the engaged body; 2) the caregivers' understanding, encouragement, and response to patients during the activity; 3) mutual tenderness and communion; and 4) environmental conditions. Results were then synthesized into a general assessment of the emotional states observed and reported in relation to the activities.Read on
Walking difficulties in patients with Alzheimer's disease might originate from gait apraxia.Read on
Wandering: a significant problem among community-residing individuals with Alzheimer's disease.Read on
Keeping wandering nursing home residents at the table: improving food intake using a behavioral communication intervention.Read on
The emotional response to social dancing and walks in persons with dementia was studied to better understand the feasibility, popularity, and meaning of these activities from the perspective of the patient. Social dance events and walks were videotaped and analyzed using Husserl's philosophy as a basis for the analysis. Six persons with dementia participated in the study. The results are described in terms of four interrelated themes: 1) the engaged body; 2) the caregivers' understanding, encouragement, and response to patients during the activity; 3) mutual tenderness and communion; and 4) environmental conditions. Results were then synthesized into a general assessment of the emotional states observed and reported in relation to the activities.Read on
Walking difficulties in patients with Alzheimer's disease might originate from gait apraxia.Read on
Wandering: a significant problem among community-residing individuals with Alzheimer's disease.Read on
Keeping wandering nursing home residents at the table: improving food intake using a behavioral communication intervention.Read on
Saturday, January 21, 2006
Dual task effects of walking when talking in Alzheimer's disease.
Rev Neurol (Paris). 2004 Jan;160(1):74-80
Authors: Cocchini G, Della Sala S, Logie RH, Pagani R, Sacco L, Spinnler H
Previous studies with Alzheimer Disease (AD) patients have suggested that speed and accuracy in walking can be dramatically affected by a simultaneous secondary cognitive task, such as holding a conversation. Two experiments examined the impact on AD patients and age matched elderly controls of cognitive demands while walking.
In Experiment 1 walking for AD patients was more affected than it was for the normal elderly by a concurrent cognitive demand.
Experiment 2 demonstrated that both groups were equally impaired under dual task conditions when the demands of the cognitive tasks were adjusted for individual levels of ability.
We conclude that walking may draw on general executive resources, that walking relies more heavily on these executive resources in the elderly, and on a damaged executive system for AD patients.
Chocolate and Prevention of Cardiovascular Disease: A Systematic Review.Read on
Managing Alzheimer's disease: global care and support program.Read on
Epidemiology of Alzheimer's disease.Read on
Friday, January 20, 2006
Researchers Find Another Origin for Alzheimer's
HealthDay News
New findings on the origins of Alzheimer's disease, if confirmed, could turn prevailing theories on their heads, researchers contend. Scientists reporting in the Jan. 18 issue of the Journal of Neuroscience said the neurodegenerative disease may be triggered when adult nerve cells, or neurons, try to divide. The work was done in mice and needs to be confirmed in subsequent studies, the researchers stressed. However, the results may provide additional insight into the early cellular events that lead to Alzheimer's in humans. "It really is going against the central grain of what we know, and it actually may lead to something more promising," said Danilo Tagle, program director in neurogenetics at the U.S. National Institute of Neurological Disorders and Stroke, which sponsored the study. Other experts are playing down the novelty of the findings. "It's another piece of the puzzle falling into place, but I would not say it debunks other theories," said Maria Carrillo, director of medical and scientific affairs at the Alzheimer's Association. "This particular piece gives more information about what cell division is doing before you get to the disease state." The prevailing theory of Alzheimer's is that it is caused by a build-up of amyloid plaques in the brain that cause neurons to divide and die. Cells divide through a process called the "cell cycle." In most cases, neurons usually do not participate in this process, however. "In regular cells, like in bone and blood, the cells divide. But brain cells do not normally divide," Tagle explained. "The great majority will not divide. The neurons you're born with are pretty much what you have at end of life." When adult nerve cells do enter this cycle, however, they will die rather than complete the division. "Cells become stuck in the process of cell division," Tagle explained. The authors of this study, based at Case Western Reserve University's Alzheimer's Disease Center in Cleveland, used mouse models to see if other processes might be at play. To that end, they compared brains cells of three different mouse models of Alzheimer's with brain cells sourced from normal mice. Alzheimer's mice showed evidence of cell cycling six months before any amyloid plaques showed up, the researchers noted. These neurons also had extra chromosomes, another sign that they had begun to divide. Most of this activity was seen in the cortex and hippocampus regions of the brain, which are most implicated in Alzheimer's. This would seem to indicate that the formation of amyloid plaques in the brains of Alzheimer's patients is more a byproduct or adjunct of the disease rather than the initiating mechanism. "The finding would indicate that there are earlier events that are happening that precede the plaque build-up," Tagle said. "The authors have demonstrated in animal models that these changes are happening as early as six months before the first signs of plaque accumulation. This seems to be a separate cellular process unlinked to the plaque process." "This overturns the central dogma of Alzheimer's disease," Tagle continued. "It opens up the possibility that this is the event that's actually triggering the cells to die. The plaques then would be like red herrings that are a secondary process, and the abnormal cellular process is primary." The next step will be to see if disrupting the cycle would cause neurons to survive. To that end, the study authors are conducting experiments to see if the painkiller ibuprofen can stop the cell cycle process, and thereby neurodegeneration. Ibuprofen, an anti-inflammatory drug, has been shown to reduce the production of amyloid-beta plaques. "That would actually lead to less cell death in Alzheimer's, so that would certainly be something that would lessen the impact of the disease," Tagle said. "This clearly supports the idea that there is more to the story," Carrillo added. "Where exactly those pieces fit, we don't know yet."
A Brisk Daily Walk May Keep the Brain Fit.Read more...
Thursday, January 19, 2006
Vitamins C and E have a beneficial effect on the development of Alzheimer
Laegeforen. 2006 Jan 12;126(2):159-61
BACKGROUND:Alzheimer dementia is a neurodegenerative disease characterised by loss of memory and other cognitive functions. Oxidative stress is a possible pathogenetic factor and the anti-oxidating vitamins C and E could therefore have a beneficial effect and reduce the damage caused by beta-amyloid.
MATERIALS AND METHODS:The relevant literature (several observational studies and two clinical controlled trials) describing effects of vitamin C and E in Alzheimer dementia have been evaluated.
RESULTS:Several observational studies in mostly healthy, elderly individuals have indicated that vitamin C and E, mainly from food as well as the combination of high doses of the same vitamins, may have beneficial effect on the development of Alzheimer dementia. One clinical controlled trial in patients with manifest Alzheimer dementia, in which vitamin E 2000 mg/day was given as the only vitamin, has to a certain extent confirmed these results.
INTERPRETATION:A causal relationship between intake of the vitamins and Alzheimer dementia has not been clarified. The correct dosages are not known, but a diet rich in these vitamin could probably reduce the risk of dementia. With a high intake of vitamin E, the addition of vitamin C is necessary.
Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older.Read on
Nitric oxide mimetic molecules as therapeutic agents in Alzheimer's disease.Read on
A potential role of the curry spice curcumin in Alzheimer's disease.Read on
Wednesday, January 18, 2006
Melatonin Benefits The Aging
BUENOS AIRES, Argentina
Melatonin normalizes sleep patterns, inhibits cognitive degeneration and protects against age-related macular degeneration (AMD) in elderly individuals, in whom endogenous melatonin production naturally decreases, according to a review authored by researchers from the University of Buenos Aires (Ann N Y Acad Sci, 1057:327–36, 2005).
In the review, researchers reported melatonin, a chronobiotic capable of shifting circadian rhythms, benefits the elderly by decreasing sleep latency and increasing sleep efficiency, resulting in increased sleep propensity and synchronization of the circadian clock. They added melatonin is of particular benefit to elderly Alzheimer's disease (AD) patients, in whom melatonin production is severely impaired, by decreasing "sundowning" agitation and reducing variability of sleep onset time. In addition, they noted open and controlled studies have indicated a significant decrease of cognitive deterioration in AD patients treated with melatonin, possibly by promoting slow-wave sleep, augmenting the restorative phases of sleep, and/or protecting neurons against beta-amyloid toxicity. The researchers concluded melatonin provides an innovative neuroprotective strategy to reduce the cost of lifetime treatment of some neuropsychiatric disorders by its combined chronobiotic and cytoprotective properties.
In the clinical trial, researchers tested the theory that supplementing aged people with melatonin may reverse the normal physiological decrease of melatonin, thereby inhibiting oxidative damage in retinal pigment epithelium (RPE) cells, a precursor of AMD, a major cause of severe visual loss in aged people. In this case-control study, 100 patients with dry or wet AMD received 3 mg/d of melatonin for at least three months. Fifty-five patients were followed for more than six months. At the six month mark, visual acuity had been kept generally stable in subjects given melatonin. Further, the researchers noted the change in the fundus (interior eye surface) picture of these patients was "remarkable." Only eight patients showed more retinal bleeding and six had more retinal exudates, while the majority of test subjects given melatonin had reduced pathologic macular changes. The researchers concluded use of 3 mg/d of melatonin seems to protect the retina and to delay macular degeneration.
In the clinical trial, researchers tested the theory that supplementing aged people with melatonin may reverse the normal physiological decrease of melatonin, thereby inhibiting oxidative damage in retinal pigment epithelium (RPE) cells, a precursor of AMD, a major cause of severe visual loss in aged people. In this case-control study, 100 patients with dry or wet AMD received 3 mg/d of melatonin for at least three months. Fifty-five patients were followed for more than six months. At the six month mark, visual acuity had been kept generally stable in subjects given melatonin. Further, the researchers noted the change in the fundus (interior eye surface) picture of these patients was "remarkable." Only eight patients showed more retinal bleeding and six had more retinal exudates, while the majority of test subjects given melatonin had reduced pathologic macular changes. The researchers concluded use of 3 mg/d of melatonin seems to protect the retina and to delay macular degeneration.
Tuesday, January 17, 2006
Exercise Significantly Reduces Risk of Dementia in Senior Citizens
A new study, and maybe the best to date, joins a growing library of information indicating that regular exercise may delay or prevent dementia in senior citizens. The new research says older adults who exercised at least three times a week were much less likely to develop dementia than those who were less active.
The study did not demonstrate directly that exercise reduces risk of dementia, but it joins a growing body of observational research pointing to an association between exercise and cognitive decline, say scientists at the National Institute on Aging (NIA), a component of the National Institutes of Health (NIH), U.S. Department of Health and Human Services, which funded the study.
The research, which will be reported in tomorrow's issue of the Annals of Internal Medicine, was conducted by Eric B. Larson, M.D., Ph.D., and colleagues at the Group Health Cooperative (GHC), the University of Washington, and the VA Puget Sound Health Care System in Seattle, WA.
Larson and co-investigators followed 1,740 GHC members age 65 or older for an average of 6.2 years between 1994 and 2003. When the study began, the participants -- all of whom were tested and found to be cognitively normal -- reported the number of days per week they engaged in at least 15 minutes of physical activity, such as walking, hiking, bicycling, aerobics, or weight training.
Their cognitive function was then assessed, and new cases of dementia were identified, every 2 years.
By the end of the study, the rate of developing dementia was significantly lower for those who exercised more -- 13.0 per 1,000 "person years" for those who exercised three or more times weekly, compared with 19.7 per 1,000 "person years" for those who exercised fewer than three times per week -- a 32 percent reduction in risk.
"Physical activity has been shown to be beneficial for health and aging in a number of areas," says Dallas Anderson, Ph.D., program director for population studies in the Dementias of Aging Branch of NIA's Neuroscience and Neuropsychology of Aging Program.
"This emerging association between exercise and cognitive health is increasingly important to understand." The NIA is beginning to support clinical trials which seek to test exercise for its direct effect on cognitive function.
Such research, Anderson says, should help sort out whether exercise reduces risk of cognitive decline or whether other factors related to exercise, such as increased social interaction, play a role. Additional study also may provide information on the possible merits of varying types of exercise.
The NIA offers a free 80-page booklet, *Exercise: A Guide from the National Institute on Aging*, which provides consumers with valuable information, including suggested exercises. The booklet and video may be ordered by calling 1-800-222-2225 or visiting the NIA Information Center Website at http://www.nia.nih.gov/HealthInformation. (The booklet can also be downloaded from the website.)
Related Stories
Evidence Growing that Alzheimer's Risk Greatly Diminished by Exercise
A new study, and maybe the best to date, joins a growing library of information indicating that regular exercise may delay or prevent dementia in senior citizens. The new research says older adults who exercised at least three times a week were much less likely to develop dementia than those who were less active.
The study did not demonstrate directly that exercise reduces risk of dementia, but it joins a growing body of observational research pointing to an association between exercise and cognitive decline, say scientists at the National Institute on Aging (NIA), a component of the National Institutes of Health (NIH), U.S. Department of Health and Human Services, which funded the study.
The research, which will be reported in tomorrow's issue of the Annals of Internal Medicine, was conducted by Eric B. Larson, M.D., Ph.D., and colleagues at the Group Health Cooperative (GHC), the University of Washington, and the VA Puget Sound Health Care System in Seattle, WA.
Larson and co-investigators followed 1,740 GHC members age 65 or older for an average of 6.2 years between 1994 and 2003. When the study began, the participants -- all of whom were tested and found to be cognitively normal -- reported the number of days per week they engaged in at least 15 minutes of physical activity, such as walking, hiking, bicycling, aerobics, or weight training.
Their cognitive function was then assessed, and new cases of dementia were identified, every 2 years.
By the end of the study, the rate of developing dementia was significantly lower for those who exercised more -- 13.0 per 1,000 "person years" for those who exercised three or more times weekly, compared with 19.7 per 1,000 "person years" for those who exercised fewer than three times per week -- a 32 percent reduction in risk.
"Physical activity has been shown to be beneficial for health and aging in a number of areas," says Dallas Anderson, Ph.D., program director for population studies in the Dementias of Aging Branch of NIA's Neuroscience and Neuropsychology of Aging Program.
"This emerging association between exercise and cognitive health is increasingly important to understand." The NIA is beginning to support clinical trials which seek to test exercise for its direct effect on cognitive function.
Such research, Anderson says, should help sort out whether exercise reduces risk of cognitive decline or whether other factors related to exercise, such as increased social interaction, play a role. Additional study also may provide information on the possible merits of varying types of exercise.
The NIA offers a free 80-page booklet, *Exercise: A Guide from the National Institute on Aging*, which provides consumers with valuable information, including suggested exercises. The booklet and video may be ordered by calling 1-800-222-2225 or visiting the NIA Information Center Website at http://www.nia.nih.gov/HealthInformation. (The booklet can also be downloaded from the website.)
Related Stories
Evidence Growing that Alzheimer's Risk Greatly Diminished by Exercise
Monday, January 16, 2006
Dual task effects of walking when talking in Alzheimer's disease.
Cocchini G, Della Sala S, Logie RH, Pagani R, Sacco L, Spinnler H
Previous studies with Alzheimer Disease (AD) patients have suggested that speed and accuracy in walking can be dramatically affected by a simultaneous secondary cognitive task, such as holding a conversation. Two experiments examined the impact on AD patients and age matched elderly controls of cognitive demands while walking. In Experiment 1 walking for AD patients was more affected than it was for the normal elderly by a concurrent cognitive demand. Experiment 2 demonstrated that both groups were equally impaired under dual task conditions when the demands of the cognitive tasks were adjusted for individual levels of ability. We conclude that walking may draw on general executive resources, that walking relies more heavily on these executive resources in the elderly, and on a damaged executive system for AD patients.
Floor patterns limit wandering of people with Alzheimer's.Read on
Neurofibrillary tangles, but not Alzheimer-type pathology, in a young boxer.Read on
Sunday, January 15, 2006
A 24-week open-label extension study of memantine in moderate to severe Alzheimer disease
http://obozrevatel.com/_site/_pic/video/hamlet.mpg
2006 Jan
Reisberg B, Doody R, Stöffler A, Schmitt F, Ferris S, Möbius HJ
OBJECTIVE: To evaluate long-term memantine treatment in moderate to severe Alzheimer disease.Design, Setting, and Patients Open-label, 24-week extension trial. Raters remained blind to the patients' initial study treatment. Patients (n = 175) were enrolled from the previous double-blind study in an outpatient setting.Intervention Twenty mg of memantine was given daily. MAIN OUTCOME MEASURES: Efficacy assessments from the double-blind study were continued and safety parameters were monitored. RESULTS: Patients who switched to memantine treatment from their previous placebo therapy experienced a significant benefit in all main efficacy assessments (functional, global, and cognitive) relative to their mean rate of decline with placebo treatment during the double-blind period (P<.05). The completion rate for the extension phase of the study was high (78%) and the favorable adverse event profile for memantine therapy was similar to that seen in the double-blind study. CONCLUSION: These results extend previous findings that demonstrated the efficacy and safety of memantine in the treatment of patients with moderate to severe Alzheimer disease. Exercise and Alzheimer’s Disease
Avoiding Dementia: Fitness and Your Brain
Exercise fights dementia and Alzheimer's disease
Saturday, January 14, 2006
Recipient-provider agreement on enacted support, perceived support, and provider personality.
Authors: Cohen JL, Lakey B, Tiell K, Neeley LC
This study examined agreement between recipients and providers about social support and personality. One hundred daughter caregivers of a parent with Alzheimer's disease and each caregiver's most important support provider independently reported supportive behaviors provided to caregivers, the perceived supportiveness of the provider, and providers' personality traits. For all indices, agreement was higher for enacted support than for perceived support and personality, which were similar to each other for some, but not all, indices of agreement. These findings support the validity of measures of enacted and perceived support.
Dissociation of neuropathology from severity of dementia in late-onset Alzheimer disease.Read on
Impaired verb fluency: a sign of mild cognitive impairment.Read on
Identification of dementia cases in the community: a Brazilian experience.Read on
Brief psychotherapy in Alzheimer's disease: randomised controlled trial.Read on
Friday, January 13, 2006
Maintain your brain
Should auld acquaintance be forgot? Not for lack of memory power. Improving your diet today may protect your brain later; here’s how:
Homegrown hormone therapy. Berries and broccoli are packed with plant hormones that may help prevent Alzheimer’s disease, Dutch researchers found. Women who ate at least 1 milligram of lignans per day — 3 ounces of berries or 7 ounces of broccoli — had 49 percent better memory scores in this study of 394 women.
Alcohol, but in moderation. Among 500 people with family risk factors for Alzheimer’s, those who averaged one or two drinks per week scored 6 percent higher at wordlist recall than those who abstained or drank less often than once a week, in research at the University of Wisconsin-Madison. Healthy daily drink limits: two for men, one for women.
No-nonsense calorie control. Excess weight may raise Alzheimer’s risk by creating insulin resistance, say University of Washington researchers. They induced the condition in 16 people and saw a 50 percent rise in levels of brain and spinal cord inflammatory chemicals and beta-amyloid protein — both suspected building blocks of Alzheimer’s.
Root for better memory
Rutabagas, turnips, parsnips, carrots and beets are packed with antioxidants, thought to fight the brain plaques and tangles of Alzheimer’s disease. Toss 1 1/2 -inch pieces of these root veggies with salt, pepper and olive oil. Bake covered for 20 minutes at 400 degrees, uncover, and bake 30 minutes longer.
The Neuropathology of Alzheimer Disease in African American and White Individuals.Read on
Familial Alzheimer disease in Latinos: interaction between APOE, stroke, and estrogen replacement.Read on
The capacity to vote of persons with Alzheimer's disease.Read on
Thursday, January 12, 2006
Treatment of Alzheimer's disease: current and future therapeutic approaches.
Rev Neurol Dis. 2004;1(2):60-9
Authors: Cummings JL
The pathophysiology of Alzheimer's disease (AD) includes the deposition of amyloid beta protein (Abeta) and the ensuing initiation of a variety of secondary processes, including tau hyperphosphorylation, excitotoxicity, oxidation, and inflammation. Nerve cell loss in structures responsible for manufacturing neurotransmitters results in a variety of neurochemical deficits. Current therapeutic approaches to the treatment of AD include cholinesterase inhibitors for mild to moderate disease, memantine for moderate to severe disease, and vitamin E or selegiline. Reduction of Abeta generation or aggregation, enhancement of Abeta removal, interruption of tau hyperphosphorylation, and the use of more efficacious antioxidant or anti-inflammatory agents represent promising therapeutic strategies currently being investigated. Improved methodologies for clinical trial design and analysis and the development of biological markers may hasten the identification of effective treatments for AD.
Wednesday, January 11, 2006
Region Of DNA Associated With Alzheimer's
11 Jan 2006
An international team of researchers, led by investigators at Washington University School of Medicine in St. Louis, are zeroing in on a gene that increases risk for Alzheimer's disease. They have identified a region of chromosome 10 that appears to be involved in risk for the disease that currently affects an estimated 4.5 million Americans. "There are a few genes that have been implicated in the development of early-onset Alzheimer's disease, but other than APOE, no genes have been found that increase risk for the more common, late-onset form of the disease," says principal investigator Alison M. Goate, D. Phil., the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry at Washington University. "The region of DNA identified in our study showed evidence of replication in four independent series of experiments. I haven't seen a putative risk factor show such consistent results since the e4 variant of the APOE gene was identified as a risk factor for late-onset Alzheimer's disease more than 10 years ago."
An international team of researchers, led by investigators at Washington University School of Medicine in St. Louis, are zeroing in on a gene that increases risk for Alzheimer's disease. They have identified a region of chromosome 10 that appears to be involved in risk for the disease that currently affects an estimated 4.5 million Americans. "There are a few genes that have been implicated in the development of early-onset Alzheimer's disease, but other than APOE, no genes have been found that increase risk for the more common, late-onset form of the disease," says principal investigator Alison M. Goate, D. Phil., the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry at Washington University. "The region of DNA identified in our study showed evidence of replication in four independent series of experiments. I haven't seen a putative risk factor show such consistent results since the e4 variant of the APOE gene was identified as a risk factor for late-onset Alzheimer's disease more than 10 years ago."
Region of DNA strongly associated with Alzheimer's disease
Natural approaches for psychological disorders
Two Pathways Found That Lead To Alzheimer's Disease
Tuesday, January 10, 2006
Alzheimer's linked to obesity
Scientists have linked diseases like Alzheimer's and kidney failure to obesity. Being overweight already exacerbates health problems heart disease and diabetes, but now another link has been made between poor health and obesity.Scientists at the University of California and the Thomas Jefferson University in Philadelphia studied data collected from over 32,000 people over a period of 26 years. They found that those who were obese were up to seven times more likely to develop kidney failure, or end-stage renal disease, than those who were of a normal weight. A "strong correlation" between obesity and the tendency to develop Alzheimer's was also discovered. The fatter the patient, the higher the levels of beta-amyloid, a sticky protein that builds up in the brain as a precursor to the disease, the research found. Dr Sam Gandy of Thomas Jefferson University announced: "Ours is one of the first attempts to try to find out on both the pathological and the molecular levels how obesity was increasing the risk of Alzheimer's."
Monday, January 09, 2006
Annually, 15 million people worldwide experience a stroke, of which 5 million are fatal and an equal number are left permanently disabled and in need of assistance for activities of daily living. In the United States alone, approximately 700 000 people have a stroke each year, of which 500 000 are first stroke events. Alzheimer disease accounts for 60% to 70% of cases of progressive cognitive impairment in elderly patients in Western societies. The prevalence of Alzheimer disease exceeds 4 million in the United States alone, and each year, 400 000 new cases are diagnosed. Assuming current trends, the numbers are expected to more than triple over the next 50 years.
Seshadri et al also evaluated the lifetime risk of stroke by blood pressure classes, suggesting that lower blood pressure in any age group is associated with lower lifetime risk of stroke, although the effect seems less apparent in older age groups. In contrast, blood pressure categories were not associated with the lifetime risk of dementia/Alzheimer. In other studies, it has been shown that elevated blood pressure in midlife is related to increased risk of Alzheimer disease. However, in late life, the relationship of blood pressure and risk for subsequent Alzheimer disease is controversial.
Sunday, January 08, 2006
New findings that long-overlooked brain cells play an important role in regulating blood flow in the brain call into question one of the basic assumptions underlying today's most sophisticated brain imaging techniques and could open a new frontier when it comes to understanding Alzheimer's disease.
Now the group led by Nedergaard, professor in the Department of Neurosurgery and a member of the Center for Aging and Developmental Biology, and post-doctoral associate Takahiro Takano, Ph.D., the first author of the paper, has thrown doubt on the assumption by showing that astrocytes are important players in the process too. Studies by the team in mice show that signaling from astrocytes causes arteries in the brain to expand, bringing about an increase in blood flow. "When we measure blood flow," said Nedergaard, "it may be that we are not measuring the activity of neurons so much as that of astrocytes." The idea creates a "chicken or egg" type question in patients with conditions like Alzheimer's or traumatic brain injury where blood flow to parts of the brain plummets. In Alzheimer's it's known that neurons sicken and die over a period of years. To diagnose the disease, doctors often order a brain scan. When the test shows lessened blood flow, doctors assume that there must be less of a demand for blood, and so significant numbers of neurons in that brain region must have died. While that still may be true, Nedergaard said, the new results muddy the picture, calling into question any straightforward link between the health of neurons and blood flow. Nedergaard said that while it is new to find that astrocytes can regulate blood flow, the finding shouldn't be entirely surprising. She said that astrocytes physically touch both synapses - the spaces between neurons that are crucial to brain activity - and blood vessels. In fact, "footprints" of astrocytes are literally all over blood vessels in the brain: Portions of astrocytes known as "astrocytic endfeet" wrap around nearly all the blood vessels in the brain.
["The disclosure had started by the signals"] Read on
Effects of Abeta immunization (AN1792) on MRI measures of cerebral volume in Alzheimer disease. Read on
Clinical effects of Abeta immunization (AN1792) in patients with AD in an interrupted trial. Read on
The Lifetime Risk of Stroke. Estimates From the Framingham Study. Read on
Saturday, January 07, 2006
The compound that gives the popular Indian spice curry its mustard yellow color may ward off Alzheimer’s disease. Curry is a dietary staple in India, a country where the rate of Alzheimer’s disease is among the world’s lowest. For centuries, doctors practicing traditional Indian medicine have safely prescribed curcumin in extract form for a variety of illnesses and ailments.
Researchers say curry’s powerful antioxidant and anti-inflammatory properties make it a very attractive possibility for treating diseases such as Alzheimer’s, cancer, and heart disease.
In studies looking at curcumin’s potential as a chemopreventive therapy, no side effects were seen in patients taking as much as 2,000 to 8,000 mg per day.
For this study, scientists raised two groups of mice, one that was fed a diet high in curcumin and the other a regular diet. Previous research in mice has shown that daily curcumin lowers plaque deposits in the brain. When fed to aged mice with advanced plaque deposits similar to Alzheimer’s disease, the curcumin reduced the amount of plaque. The scientists then injected curcumin into the brains of the mice with the Alzheimer’s-like condition. The curcumin attached to the plaques, hampering further development of plaque and reducing plaque levels.
Moreover, in other experiments, the researchers showed that curcumin reduced plaque better than the over-the-counter painkillers naproxen and ibuprofen. Some studies have shown that people taking these common anti-inflammatories have a decreased risk of developing Alzheimer’s disease.
"The prospect of finding a safe and effective new approach to both prevention and treatment of Alzheimer’s disease is tremendously exciting," Gregory Cole, MD, a professor of medicine and neurology at the David Geffen School of Medicine at UCLA, said in a news release.
Researchers say curry’s powerful antioxidant and anti-inflammatory properties make it a very attractive possibility for treating diseases such as Alzheimer’s, cancer, and heart disease.
In studies looking at curcumin’s potential as a chemopreventive therapy, no side effects were seen in patients taking as much as 2,000 to 8,000 mg per day.
For this study, scientists raised two groups of mice, one that was fed a diet high in curcumin and the other a regular diet. Previous research in mice has shown that daily curcumin lowers plaque deposits in the brain. When fed to aged mice with advanced plaque deposits similar to Alzheimer’s disease, the curcumin reduced the amount of plaque. The scientists then injected curcumin into the brains of the mice with the Alzheimer’s-like condition. The curcumin attached to the plaques, hampering further development of plaque and reducing plaque levels.
Moreover, in other experiments, the researchers showed that curcumin reduced plaque better than the over-the-counter painkillers naproxen and ibuprofen. Some studies have shown that people taking these common anti-inflammatories have a decreased risk of developing Alzheimer’s disease.
"The prospect of finding a safe and effective new approach to both prevention and treatment of Alzheimer’s disease is tremendously exciting," Gregory Cole, MD, a professor of medicine and neurology at the David Geffen School of Medicine at UCLA, said in a news release.
Friday, January 06, 2006
Gold Nanoparticles and Radiation May Slow Alzheimer's
06 Jan 2006
Chemists in Chile and Spain have identified a new approach for the possible treatment of Alzheimer's disease that they say has the potential to destroy beta-amyloid fibrils and plaque -- hypothesized to contribute to the mental decline of Alzheimer's patients. The researchers say the new technique, which they call a type of "molecular surgery," could halt or slow the disease's progress without harming healthy brain cells. The research is scheduled for publication in the Jan. 11 issue of the American Chemical Society's Nano Letters.
Chemists in Chile and Spain have identified a new approach for the possible treatment of Alzheimer's disease that they say has the potential to destroy beta-amyloid fibrils and plaque -- hypothesized to contribute to the mental decline of Alzheimer's patients. The researchers say the new technique, which they call a type of "molecular surgery," could halt or slow the disease's progress without harming healthy brain cells. The research is scheduled for publication in the Jan. 11 issue of the American Chemical Society's Nano Letters.
Using test tube studies, the scientists attached gold nanoparticles to a group of beta amyloid fibrils, incubated the resulting mixture for several days and then exposed it to weak microwave fields for several hours. The energy levels of the fields were six times smaller than that of conventional cell phones and unlikely to harm healthy cells, the researchers say. The fibrils subsequently dissolved and remained dissolved for at least one week after being irradiated, indicating that the treatment was not only effective at breaking up the fibrils but also resulted in a lower tendency of the proteins to re-aggregate, according to the researchers.
The same approach also holds promise for treating other neurodegenerative diseases that involve protein aggregation, including Parkinson's and Huntington's, says study leader Marcelo J. Kogan, of the University of Chile in Santiago. He says that the approach is similar to that of another experimental technique that uses metallic nanoparticles to label and destroy cancer cells. Animal studies are planned, Kogan says. There's currently no cure for Alzheimer's disease and no one is sure of its exact causes. The disease affects an estimated 4.5 million people in the United States, according to the National Institute on Aging. That figure is expected to rise dramatically as the population ages, experts predict.
Thursday, January 05, 2006
Exercise helps to flush a toxic molecule from the brain and causes a beneficial one to move in and protect nerve cells, research on mice shows.
"Our experiments support the idea that exercise is a good approach to all types of problems in the brain and that a sedentary lifestyle is a risk factor," says Ignacio Torres-Aleman, who led the study at the Cajal Institute in Madrid. They found that exercise doubled the levels of a protein that helps to flush molecules thought to underlie Alzheimer's disease out of the mice's brains and into their blood.
The protein, called megalin, ejects a potentially destructive protein called amyloid-beta. Megalin also binds to a beneficial molecule in the blood, called insulin-like growth factor, and transports it to the brain.
The findings appear in the Journal of Neuroscience1.
Paul Adlard, a neuroscientist at the University of California, Irvine, has looked at the brains of mice in a different model of Alzheimer's disease. His data, although only preliminary, suggest that exercise does not boost levels of the protective insulin-like growth factor. Adlard says that the findings of Torres-Aleman and his colleagues are "tantalizing", but that more study is needed. The findings, he says, open the door to developing drugs that could boost levels of the megalin shuttle and help keep the brain healthy.
Mattson notes that the link between exercise and brain health is still not certain in humans, although the evidence is mounting up. Other research has found that staying mentally agile or even maintaining a slim physique may help to protect against Alzheimer's and other brain disorders.
"Our experiments support the idea that exercise is a good approach to all types of problems in the brain and that a sedentary lifestyle is a risk factor," says Ignacio Torres-Aleman, who led the study at the Cajal Institute in Madrid. They found that exercise doubled the levels of a protein that helps to flush molecules thought to underlie Alzheimer's disease out of the mice's brains and into their blood.
The protein, called megalin, ejects a potentially destructive protein called amyloid-beta. Megalin also binds to a beneficial molecule in the blood, called insulin-like growth factor, and transports it to the brain.
The findings appear in the Journal of Neuroscience1.
Paul Adlard, a neuroscientist at the University of California, Irvine, has looked at the brains of mice in a different model of Alzheimer's disease. His data, although only preliminary, suggest that exercise does not boost levels of the protective insulin-like growth factor. Adlard says that the findings of Torres-Aleman and his colleagues are "tantalizing", but that more study is needed. The findings, he says, open the door to developing drugs that could boost levels of the megalin shuttle and help keep the brain healthy.
Mattson notes that the link between exercise and brain health is still not certain in humans, although the evidence is mounting up. Other research has found that staying mentally agile or even maintaining a slim physique may help to protect against Alzheimer's and other brain disorders.
Wednesday, January 04, 2006
Reduced Brain Volume May Predict Dementia In Healthy Elderly
04 Jan 2006
Reduced volume, or atrophy, in parts of the brain known as the amygdala and hippocampus may predict which cognitively healthy elderly people will develop dementia over a six-year period, according to a study in the January issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Reduced volume, or atrophy, in parts of the brain known as the amygdala and hippocampus may predict which cognitively healthy elderly people will develop dementia over a six-year period, according to a study in the January issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
New strategies may be able to prevent or delay the onset of Alzheimer's disease (AD), the most common cause of dementia among older adults, according to background information in the article. Accurate methods of identifying which people are at high risk for dementia in old age would help physicians determine who could benefit from these interventions. There is evidence that adults with AD and mild cognitive impairment, a less severe condition that is considered a risk factor for AD, have reduced hippocampal and amygdalar volumes. However, previous research has not addressed whether measuring atrophy using magnetic resonance imaging (MRI) can predict the onset of AD at an earlier stage, before cognitive symptoms appear.
Tom den Heijer, M.D., Ph.D., of the Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues used MRI to assess the brain volumes of 511 dementia-free elderly people who were part of the Rotterdam Study, a large population-based cohort study that began in 1990. They screened the participants for dementia at initial visits in 1995 and 1996 and then in follow-up visits between 1997 and 2003, during which they asked about memory problems and performed extensive neuropsychological testing. The authors also monitored the medical records of all participants. During the follow-up, 35 participants developed dementia and 26 were diagnosed with AD. People with severe amygdalar or hippocampal atrophy had the highest risk of developing dementia or AD over the course of the study, which followed participants for an average period of six years.
"Concerning the extent of atrophy, we found in those destined to develop dementia volume reductions between 17 percent and 5 percent, depending on how long before the diagnosis of dementia the MRI was conducted," the authors report. "In persons with mild to moderate Alzheimer disease, volume reductions compared with healthy elderly persons are between 25 percent and 40 percent, suggesting that atrophy rates accelerate in patients with Alzheimer disease." "Our study suggests that structural brain imaging can help identify people at high risk for developing dementia, even before they have any memory complaints or measurable cognitive impairment," they write. "However, we must bear in mind that most people with atrophy did not develop dementia, even after six years. Further prospective population studies are therefore required to find additional biomarkers, including other brain imaging parameters, that alone or in combination with clinical and genetic characteristics can help separate those who are at risk for developing dementia from those who are not."
Tuesday, January 03, 2006
Exercise - NEW YEAR's RESOLUTION
Physical activity appears to inhibit Alzheimer's-like brain changes in mice, slowing the development of a key feature of the disease. A study earlier this year shows long-term physical activity enhanced the learning ability of mice and decreased the level of plaque-forming beta-amyloid protein fragments - a hallmark characteristic of Alzheimer's Disease (AD) - in their brains.