NaCMed has recently partnered with Valerie Hopson-Bell, of ElderCare Connections to provide case management and advocacy assistance for patients and their families who are struggling with navigating the medical system, multiple appointments, resources and avenues for care, as well as general well being. She is closely aligned with the Rappahannock Area Agency on Aging and other agencies in the Rappahannock/Rapidan Community area and provides services in patient homes, NaCMed offices and in her own home. Please call if you are interested in services.
By Michael Smith, North American Correspondent, MedPage Today
Published: April 01, 2013
Reviewed by F. Perry Wilson, MD, MSCE; Instructor of Medicine, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner
· Note that this analysis of a large cohort study demonstrated that cognitive decline could be predicted better by Framingham cardiovascular risk scores than a specific dementia risk score.
· Be aware that the dementia risk score performed better in terms of predicting decline in memory -- suggesting it may be an appropriate tool to examine risk of Alzheimer's dementia.
Standard risk prediction tools for heart disease and stroke are better at predicting declining mental powers than a specific dementia risk score, researchers reported.
In a long-running cohort study, higher risks on the widely used Framingham cardiovascular disease and stroke scores were strongly associated with declines on four out of five cognitive tests, according to Sara Kaffashian, PhD, of the French National Institute of Health and Medical Research in Paris, and colleagues.
On the other hand, higher risk on the recently proposed Cardiovascular Risk Factors, Aging and Dementia (CAIDE) score was less strongly associated with declines and only on three of the five tests, Kaffashian and colleagues reported in the April 2 issue of Neurology.
All of the risk scores predict cognitive decline starting in late middle age, Kaffashian said in a statement, but the Framingham tests may have an edge in prevention.
"Cardiovascular risk scores may have an advantage over the dementia risk score for use in prevention and for targeting changeable risk factors since they are already used by many physicians," she said.
The varied outcomes, though, might reflect differences in the type of dementia being measured, commented Michael Rafii, MD, PhD, of the University of California San Diego.
"The measures that are being looked at with the stroke measures are more reliable in predicting vascular dementia than Alzheimer's disease, " he told MedPage Today, while the "dementia tool seems to be less correlated with vascular dementia down the road."
The exception is in memory decline, Rafii said, where the Framingham stroke tool performed less well than the CAIDE test. "And that memory decline is really the hallmark of Alzheimer's disease dementia," he said.
The study involved 7,830 participants in the Whitehall II study, who had an average age of 55 when they entered the longitudinal British cohort.
The researchers were able to compare the performance of the CAIDE test with the Framingham cardiovascular tool in 4,374 participants who were free of cardiovascular disease. They compared the CAIDE test with the stroke tool in 5,157 people free of strokes and transient ischemic attacks.
They tested participants in four cognitive domains -- reasoning, memory, verbal fluency (using two tests), and vocabulary -- three times over a 10-year period. As well, they created global cognition scores by combining results from the four domains.
On both the Framingham tools, higher scores at baseline were associated with greater decline on all tests except memory, they found. On the other hand, a higher CAIDE risk was associated with greater decline in reasoning, vocabulary, and global cognition.
Kaffashian and colleagues cautioned that the study is based on a "cohort of office-based employees that may not be entirely representative of the general population."
As well, they noted, participants had a favorable risk profile, so that the reported associations may be underestimates.
On the other hand, the study was well designed and relatively large, so the results are likely to be "meaningful," Rafii commented.
"What would have made this an even stronger study," he said, "would be further gold-standard diagnoses – for example, brain imaging, pathological specimens, or any other validated biomarkers that represent true dementia and its underlying causes."
The study had support from Région Ile-de-France, the Medical Research Council, the British Heart Foundation, the Health and Safety Executive, the French Department of Health, the National Heart, Lung and Blood Institute, the NIH, the National Institute on Aging, the Agency for Health Care Policy Research, and the John D. and Catherine T. MacArthur Foundation.
The authors did not report financial links with industry.
Primary source: Neurology
Kaffashian S, et al "Predicting cognitive decline: A dementia risk score vs the Framingham vascular risk scores" Neurology 2013; 80: 1300–1306.
By James Gallagher Health and science reporter, BBC News Can brain cell death be prevented in a range of diseases? Continue reading the main story Related Stories
In a study, published in Nature, they prevented brain cells dying in mice with prion disease.
It is hoped the same method for preventing brain cell death could apply in other diseases.
The findings are at an early stage, but have been heralded as "fascinating".
Many neuro-degenerative diseases result in the build-up of proteins which are not put together correctly - known as misfolded proteins. This happens in Alzheimer's, Parkinson's and Huntington's as well as in prion diseases, such as the human form of mad cow disease.
Turn off Researchers at the University of Leicester uncovered how the build-up of proteins in mice with prion disease resulted in brain cells dying.
They showed that as misfolded protein levels rise in the brain, cells respond by trying to shut down the production of all new proteins.
It is the same trick cells use when infected with a virus. Stopping production of proteins stops the virus spreading. However, shutting down the factory for a long period of time ends up killing the brain cells as they do not produce the proteins they actually need to function.
Continue reading the main story “Start Quote There are good reasons for believing this response, identified with prion disease, applies also to Alzheimer's and other neuro-degenerative diseases”
Prof Roger Morris King's College London The team at the Medical Research Council laboratory in Leicester then tried to manipulate the switch which turned the protein factory off. When they prevented cells from shutting down, they prevented the brain dying. The mice then lived significantly longer.
Each neuro-degenerative disease results in a unique set of misfolded proteins being produced, which are then thought to lead to brain cells dying.
Prof Giovanna Mallucci told the BBC: "The novelty here is we're just targeting the protein shut-down, we're ignoring the prion protein and that's what makes it potentially relevant across the board."
The idea, which has not yet been tested, is that if preventing the shut down protects the brain in prion disease - it might work in all diseases that have misfolded proteins.
Prof Mallucci added: "What it gives you is an appealing concept that one pathway and therefore one treatment could have benefits across a range of disorders.
"But the idea is in its early stages. We would really need to confirm this concept in other diseases."
'Fascinating' Alzheimer's brain on the left showing shrinkage, with a healthy brain on the right The study has been broadly welcomed by other scientists although many point out that the research is in its infancy.
Professor of Molecular Neurobiology at King's College London, Roger Morris, said it was a "breakthrough in understanding what kills neurons".
He added: "There are good reasons for believing this response, identified with prion disease, applies also to Alzheimer's and other neuro-degenerative diseases.
"And because it is such a general response, we already have some drugs that inhibit this response."
Prof Andy Randall, from the University of Bristol, said: "This is a fascinating piece of work.
"It will be interesting to see if similar processes occur in some of the common diseases with such deposits, for example Alzheimer's and Parkinson's disease.
"Furthermore, if this is the case, can modulating this same pathway be a route to new therapeutic approaches in these more prevalent conditions that afflict many millions of sufferers around the world? Ultimately only more research will tell us this."
Dr Eric Karran, the director of research at Alzheimer's Research UK, said: "The findings present the appealing concept that one treatment could have benefits for a range of different diseases; however the idea is in its early stages.
"The research focuses on the effects of the prion protein and we would need to see the same results confirmed in Alzheimer's and Parkinson's to really strengthen the evidence."
ScienceDaily (Apr. 4, 2009) — Investigators at Burnham Institute for Medical Research (Burnham) have demonstrated that attacks on the mitochondrial protein Drp1 by the free radical nitric oxide—which causes a chemical reaction called S-nitrosylation—mediates neurodegeneration associated with Alzheimer's disease. Prior to this study, the mechanism by which beta-amyloid protein caused synaptic damage to neurons in Alzheimer's disease was unknown.
Original Article Published: 22 August 2012
Size really does matter according to scientists looking for ways to cure Alzheimer's disease.
Research conducted by scientists at the Queensland Brain Institute (QBI) at The University of Queensland (UQ) and Harvard University, has led to the discovery that treatment for Alzheimer's disease may lie in modifying the length of subcellular structures in the brain responsible for metabolizing energy, mitochondria.
The study found in cases where the mitochondria were abnormally long, they had a toxic effect inducing cell death.
Director, Centre for Ageing Dementia Research (CADR) at QBI and co-author of the paper, Professor Jürgen Götz, said:
“Alzheimer's disease belongs to a group of neurodegenerative diseases termed ‘tauopathies', charaterised by clumps of the protein tau inside neurons.
“In instances where neurons express toxic levels of human tau, the mitochondria are elongated.
“All cells rely on mitochondria for energy metabolism, and neurons in particular, so controlling the length of these subcellular structures is very important for brain function.”
The research provides novel targets for therapeutic intervention.
“Treatments currently available for these diseases have at most modest effects, in part due to our limited understanding of how Alzheimer's disease starts and progresses,” Professor Götz said.
The good news is, genetic and drug interventions aimed at reducing mitochondrial length reverse the toxic effects of tau, and can now get underway.
“An aspect of mitochondrial regulation that is being increasingly appreciated are changes in size and shape of the organelle, through a process termed 'mitochondrial dynamics',” Professor Götz said.
Alzheimer's disease affects almost 280,000 Australians. This number grows by 1,600 each week and is expected to reach over 1 million people by 2050 .
Interview talent: Prof. Jürgen Götz
Foundation Chair of Dementia Research
Director, Centre for Ageing Dementia Research (CADR) at the Queensland
Brain Institute (QBI), The University of Queensland
Media contact: Mikaeli Costello
Queensland Brain Institute
0401 580 685
A program of Alzheimer's Association Fredericksburg Chapter
2017 Plank Rd
Fredericksburg, VA 22401
Program Type Support Group-Caregivers, Support Group-Disability/Health
Web site www.alz.org/grva/
Intake Contact Branch Coordinator Lori Myers
Intake Phone 540 370-0835
Intake Email email@example.com
Who Are We? Offers support groups to provide emotional support and care giving tips for those caring for family members with Alzheimer's disease and other dementia's.
Who Do We Serve?
Age range No age limitation
Among our staff, we can speak English
Program's target population Alzheimer's Disease
Program is able to accommodate Wheelchair, Dementia/Alzheimer's, Caregivers
Service Area (Counties) Caroline County, Fredericksburg City, Spotsylvania County, Westmoreland County
Other Eligibility Requirements Alzheimer's caregivers and friends
How Much Does Our Service Cost? No Fee
What Is Our Availability? N/A
Hours of operation
Comments: Meets 3rd Tuesday at 1:30 pm
Accessing Services Self referral. Call for information. Expect to be contacted within 24 hours. Consumer can self refer. Service provider can refer directly.
Where Service Is Provided On site
Is Your Facility:
-ADA (Americans with Disabilities Act) Compliant? Yes Fully
-Accessible to Public Transportation? Yes
-Provides Transportation to/from Service? No
-Business Type Private, Non-profit
Info taken from the alzheimers website
Can Alzheimer's be prevented? It's a question that continues to intrigue researchers and fuel new investigations. There are no clear cut answers yet — partially due to the need for more large-scale studies — but promising research is under way. The Alzheimer's Association continues to fund studies exploring the influence of mental fitness, physical fitness, diet and environment. As the number of people affected by Alzheimer's rises, the effort to find prevention strategies continues to gain momentum.
For example, as development of potentially disease-modifying drugs continues, genetic testing could one day become a valuable tool to identify individuals who might benefit from early, proactive intervention to reduce risk. Currently, routine clinical testing for Alzheimer's genes is not recommended, since no preventive treatments are available.
Learn more about the drug treatment horizon
Heart–head connection The risk of developing Alzheimer's or vascular dementia appears to increase as a result of many conditions that damage the heart or blood vessels. These include high blood pressure, heart disease, stroke, diabetes and high cholesterol. Some autopsy studies show that as many as 80 percent of individuals with Alzheimer's disease also have cardiovascular disease.
A longstanding question is why some people develop hallmark Alzheimer's plaques and tangles but do not develop the symptoms of Alzheimer's. Vascular disease may help researchers eventually find an answer. Autopsy studies suggest that plaques and tangles may be present in the brain without causing symptoms of cognitive decline unless the brain also shows evidence of vascular disease. Many experts believe that controlling cardiovascular risk factors may be the most cost-effective and helpful approach to protecting brain health.
Brain food Some of the strongest current evidence links brain health to heart health. Your brain is nourished by one of your body's richest networks of blood vessels. Every heartbeat pumps about 20 to 25 percent of your blood to your head, where brain cells use at least 20 percent of the food and oxygen your blood carries.
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Physical exercise and diet Regular physical exercise may be a beneficial strategy to lower the risk of Alzheimer's and vascular dementia. Some evidence suggests exercise may directly benefit brain cells by increasing blood and oxygen flow. Even stronger evidence suggests exercise may protect brain health through its proven benefits to the cardiovascular system. Because of the known cardiovascular benefits, a medically approved exercise program is a valuable part of any overall wellness plan.
Like exercise, diet may have its greatest impact on brain health through its effect on heart health. The best current evidence suggests that heart-healthy eating patterns, such as the Mediterranean diet, also may help protect the brain. A Mediterranean diet includes relatively little red meat and emphasizes whole grains, fruits and vegetables, fish and shellfish, and nuts, olive oil and other healthy fats.
Diet and Exercise in Alzheimer's (approx 17 min.) Catalyst to progress The Alzheimer's Association was among the first to encourage investigation of the impact of vascular factors on Alzheimer's disease. We have funded such studies for more than 20 years and continue to highlight this promising avenue of research into potentially modifiable risk factors. Learn more about our commitment to research.
Social connections and intellectual activity A number of studies indicate that maintaining strong social connections and keeping mentally active as we age might lower the risk of cognitive decline and Alzheimer's. Experts are not certain about the reason for this association. It may be due to direct mechanisms through which social and mental stimulation protect the brain. Alternatively, people who eventually develop Alzheimer's may feel less inclined to engage in socially and intellectually stimulating activities years before current diagnostic methods can detect symptoms.
Catalyst to progress Animal studies can be especially helpful in increasing our knowledge about direct mechanisms through which physical and mental stimulation may benefit the brain. Orly Lazarov, PhD, received a 2007 Alzheimer's Association New Investigator Research Grant to explore the impact of physical activity and an enriched environment on mice genetically engineered to carry one of the human genes that causes Alzheimer's disease. Her results showed that physical and mental stimulation appear to decrease hallmark Alzheimer's pathologies and support new nerve cell growth and better cell-to-cell communication.
Head trauma There appears to be a strong link between future risk of Alzheimer's and serious head trauma, especially when injury involves loss of consciousness. You can help reduce your risk of Alzheimer's by protecting your head.
What you can do now While research is not yet conclusive, certain lifestyle choices, such as physical activity and diet, may help support brain health and prevent Alzheimer's. Many of these lifestyle changes have been shown to lower the risk of other diseases, like heart disease and diabetes, which have been linked to Alzheimer's. With few drawbacks and plenty of known benefits, healthy lifestyle choices can improve your health and possibly protect your brain.
Learn more about brain health.
You can help increase our knowledge by considering participation in a clinical study. Prevention and risk management studies need healthy participants who are willing to make a long-term commitment to moving the field forward. You can find prevention trials currently recruiting in our new TrialMatch tool.
Understanding prevention research Here are some things to keep in mind about the research underlying much of our current knowledge about possible prevention:
Selected reports and resources