About 20% of Canadians over 65 are suffer from Alzheimer’s

We have all heard of age related health problems and diseases like kidney failures, cardio-vascular problems, Parkinson’s disease, senility and memory losses leading to dementia that affect the elderly. Alzheimer’s is just another form of dementia, which leads to progressive memory loss. There are many ways in which we can help those suffering from such debilitating diseases and assist them to lead quality lives in their sunset years. About 20% of Canadians above the age of 65 are suffering from Alzheimer’s according to a survey. So, there are many research studies being done about the causes and the spread of the disease. Properly understanding the causes and the way it affects the patients’ brain cells can help the researchers to develop better drugs and the doctors to come up with better ways of treating it.

A recent study done by a research team in the University of Michigan suggests that certain sizes of the ‘clumps’ of proteins seem to be detrimental to the brain cells around them, as they ‘prick’ holes in the neurons. The team has also found that the smaller clumps or larger clumps seem to have no negative effect at all. This research was recently published in the online journal, Public Library of Science One. Many scientists believe that this latest research will provide an impetus to pharmaceutical companies to come up with a drug to fight the disease as we now know how it affects the brain cells.

In the research paper titled ‘Multivariate analyses of amyloid-beta oligomer populations’ indicate a connection between pore formation and cytotoxicity’, the leader of the research team, Prof. Michael Mayer claims that the mid-length aggregates or clumps of the protein amyloid-beta peptides, are the most dangerous as they prick holes into the neurons surrounding them, with prolonged exposure. Working with eminent scientists from the University of California, San Diego, Prof. Mayer and his team have establsihed that the protein amyloid beta peptide, in certain aggregates is toxic and affects the synaptic plasticity of neurons, which means it punches holes in the cell membranes. This leads to uncontrolled flow of calcium ions, which in turn affects the communication between neurons. This result is supported by evidence gathered from autopsy reports conducted on patients with Alzheimer’s which show extracellular plaque formation in their brains.

And the research has brought another startling fact to light. The popular generic medicine Bapineuzumab, administered to patients suffering from Alzheimer’s has come under scrutiny. The drug is meant to prevent larger aggregates of the protein, which have been proved to be benign. In fact, the team working under Prof. Mayer, who heads the Bio-Medical department and also lectures in Chemical Engineering, has conducted research which suggests that smaller and larger clumps of the protein might inhibit the flow of calcium ions and actually slow down the cell degeneration.

A student and researcher under Prof. Mayer has established that the size range of amyloid clumps which formed the most pores, were also the most toxic; in the culture samples that used lipid membranes to mimic cell membranes, studied from 0 – 20 days, the resulting correlation between the aggresive pore-forming clumps and their toxicity was astounding. Further using sophisticated statistical models, the team was able to conclude that the pore-formation by certain aggregates of the amyloid-beta is responsible for cell-death in neurons.

In another research study done by the University of Haifa, the focus was on understanding the mechanisms which lead to Alzheimer’s as a result of molecular response to the metabolic distress that occurs with advancing years. In a study published in the Neurobiology of Ageing, the Department of Neurobiology team has establlsihed a firm link between the protein eIF2alpha and Alzheimer’s disease. The study, co-authored by a Canadian team claims that it is possible to prevent or even reverse the loss of cognitive abilities in Alzheimer’s patients, by regulating the eIF2alpha protien as it is responsible for the creation of protein in all cells. There are many teams around the world researching the protein now in a bid to come with a way to treat Alzheimer’s even after the patient’s memory has been affected. About The Author Dr. David Tal likes to write about Alzheimer’s and can be seen at the following sites: www.agemattersclinic.com/

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