Archive for May, 2011

Researchers at the Research Institute of the McGill University Health Centre (MUHC) have discovered a new blood test to diagnose Alzheimer’s disease (AD) which was published in the May issue of the Journal of Alzheimer’s Disease.  They have found a distinctive biochemical diagnosis in AD patients according to senior author Dr. Vassilios Papadopoulos.

Papadopoulos reports that post-mortem analysis of brain tissue has been the only definitive tool for AD. Now this clinical study shows that a non-invasive blood test based on a chemical process may be able to diagnose Alzheimer’s disease at an early stage and could be differentiated from other types of dementia.

This blood test is based on the production of a brain hormone called dehydroepiandrosterone (DHEA) which is present at high levels and has a wide range of biological effects. The researchers used a chemical process called oxidation to promote the production of DHEA in blood taken from non-Alzheimer’s patients. However, blood from AD patients did not produce an increase of DHEA.

The researchers were able to accurately and repetitively detect AD with small samples of blood. Although there are many possible therapies in clinical trials, there must first be an accurate diagnosis. Together with clinical findings, the blood test could be used to diagnose AD at a very early stage and the appropriate therapies could be monitored.

Source: MUHC Newsroom

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As a person advances in age, the brain can lose up to 10% of its original weight. The brain compensates for the loss of the cells through redundancy and plasticity mechanisms. Sylvie Belleville, Ph.D., Research Director of the Institut universitaire de geriatrie de Montreal, has discovered that elderly individuals who have a high risk of suffering from Alzheimer’s disease may find hope in the brain’s plasticity mechanism.

Brain plasticity, according to Belleville, is the brain’s ability to modify itself and reorganize in order to adapt. The traditional view is that the brain’s plasticity declines with age, but a study headed by Belleville and published online through Brain: A Journal of Neurology shows that this is not true at all, even at the onset of Alzheimer’s disease.

The new findings are promising in the field of Alzheimer’s treatment and have the potential of encouraging new research into methods, therapies, treatments and medications that can improve the brain’s plasticity, thereby reducing the number and severity of Alzheimer’s disease in patients.

The study also shows that, at least hypothetically, cells known to promote the function of certain brain processes can take over using programs designed to train and enhance memories. For Belleville, the study simply validated that hypothesis. In the study, it was noted that subjects with MCI (mild cognitive impairment) who underwent memory tests after training had increased their correct answers by 33%. MCI is known to significantly increase an individual’s risk of developing dementia.

The program used a variety of strategies to train the subjects, such as encoding, retrieval and mnemonics. There were 30 participants in the study – half of them with MCI. The other group comprised of healthy adults. Using MRI, the subjects’ brain activities were monitored and analyzed at different times during the study – six weeks before training, one week before training and one week post-training. A comparison of brain activity using MRI showed activation in the brain areas that were known to work when used in memory exercises. Activation decreased in participants with MCI as expected but after training, brain activity increased not just in the memory areas but also in those associated with spatial, skill and object memory and language processing. This shows promise in future Alzheimer’s treatment and research.

Source: UdeMNouvelles

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In a study published in mid-March in The Journal of Neuroscience Research, results from a Scripps Research Institute and ModGene, LLC study could completely change the direction of Alzheimer’s Disease (AD) research. The study points to the liver instead of the brain as the source of the “amyloid” that deposits as brain plaques associated with AD. The findings could offer a relatively simple approach for Alzheimer’s prevention and treatment.

In the study, the scientists used mice to identify genes that influence the amount of amyloid that accumulates in the brain. They found three genes that protected mice from brain amyloid accumulation and deposition. In each of those genes, lower expression in the liver protected the mouse brain. However, one of the genes encodes presenilin—a cell membrane protein believed to contribute to the development of human Alzheimer’s.

According to Scripps Research Professor Greg Sutcliffe who led the study, higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer’s-like pathology. This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain.

The study, Peripheral reduction of β-amyloid is sufficient to reduce brain Αβ: implications for Alzheimer’s disease, was also authored by Peter Hedlund and Elizabeth Thomas of Scripps Research, and Floyd Bloom and Brian Hilbush of ModGene, LLC, which funded the project. This could possibly shift the direction of Alzheimer’s Disease research.


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