Family members and close friends are more sensitive to early signs of Alzheimer’s dementia than traditional screening tests, according to researchers at Washington University School of Medicine in St. Louis.
Doctors often evaluate a person who is having memory problems by testing them with a variety of cognitive tasks, such as recalling a list of words or comparing shapes of objects. Washington University researchers developed a different approach. The two-minute Ascertain Dementia 8 (AD8) questionnaire relies on a friend or family member who knows the person well, known as an informant, to evaluate whether cognitive changes have caused the individual to have difficulties in performing everyday activities.
In the new study, published online in the journal Brain, scientists validated the AD8 by checking to see if it could highlight individuals who had biological indicators, or biomarkers, for Alzheimer’s disease, such as abnormal levels of certain factors in the spinal fluid or positive brain scans for Alzheimer’s plaques. The AD8′s results corresponded with biomarker results more consistently than traditional cognitive tests.
Alzheimers
“It’s not economically feasible to screen everyone for Alzheimer’s disease biomarkers,” says John C. Morris, MD, director of the Charles F. and Joanne Knight Alzheimer’s Disease Research Center at Washington University School of Medicine. “The AD8 gives us a brief and very low-cost alternative that takes a few minutes of the informant’s time to screen for dementia and thus identify those individuals who need follow-up evaluations to determine if there truly are signs of Alzheimer’s.”
According to Morris, the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology, the difficulty with traditional early-stage dementia screening tools is that they only give a snapshot of a person’s cognitive abilities at one point in time — when they’re being tested. Asking the individual if his or her mental abilities have changed doesn’t necessarily produce accurate results either, Morris says, because persons with early-stage dementia often lack insight into their problem.
Researchers at the Knight Alzheimer’ s Disease Research Center, including first author James Galvin, MD, now at New York University, developed the AD8 from the Center’s existing research tools. Informants are asked to rate whether there has been a change in the following areas:
* Problems with judgment, such as bad financial decisions;
* Reduced interest in hobbies and other activities;
* Repeating of questions, stories or statements;
* Trouble learning how to use a tool or appliance, such as a television remote control or a microwave;
* Forgetting the month or year;
* Difficulty handling complicated financial affairs, such as balancing a checkbook;
* Difficulty remembering appointments; and
* Consistent problems with thinking and memory.
Informants can respond yes or no to each item; each “yes” response is worth a point, and a score of two or more indicates a need for additional evaluation.
According to Morris, informants who have regular exposure to the individual provide the most accurate assessments.
“These informants can give us the retrospective perspective we need to know that a person’s mental abilities have begun to meaningfully decline, indicating that additional testing is needed,” Morris says.
For the new study, researchers gathered AD8 evaluations on 251 individuals and also tested them using the Mini Mental State exam, a traditional dementia screening test. They then evaluated biomarkers in the individuals, including spinal fluid assays and brain plaque scans.
“Based on our results, the AD8 appears to be superior to conventional testing in its ability to detect signs of early dementia,” Morris says. “It can’t tell us whether the dementia is caused by Alzheimer’s or other disorders, but it lets us know when there’s a need for more extensive evaluations to answer that question.”
Since its development, the AD8 has been translated into several different languages and validated in those languages. It is currently in use in clinics around the world.
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Researchers have successfully created an experimental vaccine against the small protein that forms plaques in the brain and is believed to contribute to the development of Alzheimer’s disease.
Compared with similar so-called DNA vaccines that the UT Southwestern researchers tested in an animal study, new study states experimental vaccine stimulated more than 10 times as many antibodies that bind to and eliminate beta-amyloid.
“The antibody is specific; it binds to plaque in the brain. It doesn”t bind to brain tissue that does not contain plaque. This approach shows promise in generating enough antibodies to be useful clinically in treating patients,” said Roger Rosenberg, senior author of the study.
The next step in the research is to test long-term safety in animals, Dr. Rosenberg said.
“After seven years developing this vaccine, we are hopeful it will not show any significant toxicity, and that we will be able to develop it for human use,” he added.
The results appeared in the journal Vaccine.
Scientists have determined how iron contributes to the production of brain-destroying plaques found in Alzheimer’s patients.
The team from Massachusetts General Hospital researchers reports that there is a very close link between elevated levels of iron in the brain and the enhanced production of the amyloid precursor protein, which in Alzheimer”s disease breaks down into a peptide that makes up the destructive plaques.
Dr. Jack T. Rogers, the head of the hospital”s neurochemistry lab who oversaw the team”s work, said the findings “lay the foundation for the development of new therapies that will slow or stop the negative effects of iron buildup” in patients with the progressive neurodegenerative disease, symptoms of which include memory loss, impaired judgment, disorientation and personality changes.
While it had been known that an abundance of iron in brain cells somehow results in an abundance of amyloid precursor protein, or APP, and its destructive peptide offspring, Rogers” team set out to open up new avenues for therapies by determining what goes on at the molecular level.
In 2002, they identified the molecular location where APP and iron interact, a discovery that laid the groundwork for the work being reported now.
Today it is clear that, under healthy conditions, iron and APP keep each other in check: If there”s too much iron in a brain cell, more APP is made, and then APP and a partner molecule escort excess iron out.
And, as the team reported last month in a related paper in the journal Cell, if there”s too little iron, fewer APP molecules are made available to help escort iron out. As a result, iron accumulates, and the process begins again in a feedback loop.
Rogers said the team”s work detailed in the two recent papers “seals the loop” in what has been understood about APP and iron and paves the way for the development of drugs that will beef up the ability of APP and its partner to eject iron and restore the iron balance when needed.
The researchers also identified, in the JBC paper, another important player in the system of checks and balances used to regulate iron in brain cells. Known as IRP1, which stands for iron-regulating protein 1, the special molecule attaches to the messenger RNA that holds the recipe for making APP.
When there”s less iron in the brain cell, IRP1 is more likely to hook up with the RNA, which prevents the production of APP. When there”s abundant iron present, IRP1 doesn”t hook up with the RNA, and APP production becomes excessive.
The new information solidified the team”s hunch that the particular region where IRP1 binds to the messenger RNA is a potential drug target.
“With other research teams, we are investigating novel therapies that remove excessive iron, and we”re looking at the precise spot on the messenger RNA where IRP1 binds to screen for drugs that specifically prevent APP production,” said Dr. Catherine Cahill, one of the lead authors.
The study results appear in this week”s Journal of Biological Chemistry.
Vulnerable elderly people are being unfairly forced to pay for health care, the new chairman of the House of Commons health committee says.
Stephen Dorrell said patients with conditions such as dementia used to get free care in NHS geriatric hospitals.
But the number of places has fallen by nearly 80% in the UK over the past 20 years – despite the ageing population.
He said this had pushed people into the means-tested social care system where they were often charged for treatment.
In an interview with the BBC, he said the redrawing of the boundaries had been allowed to creep in without proper debate or scrutiny and urged politicians to face up to the issue.
An expert commission has already been set up by the government to look into the issue of social care funding in England.
But Mr Dorrell was speaking about a specific group of patients whom he believes the NHS has turned its back on.
As well as dementia patients this includes people such as stroke victims and those with Parkinson’s disease who struggle to get the NHS to pay for medical treatment they receive.
Mr Dorrell, who was health secretary towards the end of John Major’s time as prime minister, said: “People are being charged for care that they would have got free from the NHS 20 or 30 years ago.
“In effect there has been a change in the definition of what constitutes NHS care and that has happened without proper debate.
“Unfortunately, it has been ignored because both politically and financially it is tricky for politicians to face up to it. But because it has not been done in a planned way there is great unfairness in the system. We see examples of cost shunting and bureaucracy that cause individuals problems.
http://www.bbc.co.uk/news/health-11429779
Alzheimer’s disease (AD) patients suffering from high blood pressure may have a reduced blood flow to the brain. Decreased blood flow probably leads to worse form of dementia. Investigators from the Bristol University have found a possible relationship between dementia, high blood pressure and blood flow in the brain. The findings can help scientists in developing drugs for treating diseases like stroke and Alzheimer’s.
Scientists evaluated if drugs blocking a small naturally produced molecule called endothelin-1 (ET-1) can boost blood flow through the brain. Animal models with AD were analyzed by the investigators. It appeared that reduction in blood flow took place before the onset of Alzheimer-like damaging alterations to brain tissue. Endothelin-1 is apparently regarded as the most dominant cause of narrowing blood vessels. The action of endothelin-converting enzymes (ECEs) seemingly produces ET-1.
“We hope our study will shed light on the role of amyloid ?. We know it to be involved in AD but it is produced throughout life and what it does in the normal brain has long been a mystery. In addition, our research could have important implications for blood pressure control in people with hypertension as well as for treatment of diseases such as stroke and dementia where effective treatments remain limited. Drugs that block ET-1 are already licensed for the treatment of other human diseases and could be used to treat people who have elevated levels of amyloid ? and increased ECE-2 activity, whether in the context of established AD or stroke, or at an earlier stage prior to the development of irreversible brain damage,” explained Seth Love, Professor of Neuropathology.
Experts claim to have found significant amount of ECE-2 in the brain of AD patients. Amyloid ? which is a toxic molecule gathering in the brain of AD patients seems to be a hallmark of the disease. It was demonstrated that ECE-2 production heightened when nerve cells were exposed to amyloid ?. This process apparently occurred before people start to display the memory problems recognized in AD. It is assumed that blood flow through the brain in AD is reduced due to an increase of ET-1, from the stimulatory effect triggered by amyloid ? on ECE-2 production.
The research was funded by British Heart Foundation (BHF).
A research team led by Mount Sinai School of Medicine has identified the mechanism behind a single gene linked to the causes of both Alzheimer’s disease and Type 2 diabetes. The data show that a gene for a protein called SorCS1, which can cause Type 2 diabetes, impacts the accumulation of amyloid-beta (Abeta) in the brain. Abeta plays a key role in the development of Alzheimer’s disease.
The study is published in the September 29th issue of the Journal of Neuroscience.
Sam Gandy, MD, PhD, the Mount Sinai Professor in Alzheimer’s Disease Research, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer’s Disease Research Center at Mount Sinai School of Medicine, led the study, together with first author Rachel Lane, PhD, a postdoctoral researcher in Gandy’s Lab. Lane and Gandy analyzed both the brains of mice genetically engineered to be deficient in SorCS1 as well as cells engineered to express high levels of SorCS1. They found an increased level of Abeta in SorCS1-deficient mice, and low levels of Abeta in the cells overexpressing SorCS1.
“We knew that Type 2 diabetes could increase the risk for Alzheimer’s disease, but we were not sure how that risk was caused or whether that diabetes risk would impact Abeta levels in the brain,” said Dr. Gandy. “These results elucidate a common mechanism between diabetes and Alzheimer’s and will bring us a step closer to identifying effective treatments for both diseases.”
http://www.sciencedaily.com/releases/2010/09/100928171553.htm