Alzheimer’s disease is a neurodegenerative disease that I took interest in because people spend their whole lives using cognitive function to create who they are. For some people the latter years of life are spent loosing all that function that was meticulously fostered to define them.
Alzheimer’s is the most common cause for Dementia, its cause and progression are not clearly known and there are no treatments for the disease. Despite a lack of options, there are a few things that are known about Alzheimer’s, such as the target population, the general symptoms and the plaque and tangle significance.
The disease targets people who are 65 and older. The progression can go from 5 years to 20 years and unless symptoms are displayed it the beginning stages can be overlooked. The most common symptom that brings the disease to light is memory loss becomes a concern to the individual. Other symptoms that follow are mood swings, confusion, anger and long-term memory loss. Individuals that have been diagnosed with Alzheimer’s are associated with having large numbers of plaques and tangles in the brain. Plaques are extracellular deposits in the gray matter of the brain that are surrounded by an abundance of immune cells microglia and astrocytes that are associated with neural degenerative disease. Tangles are protein aggregates also seen in those with Alzheimer’s however their role is unknown.
Perhaps with further research new strides can be made.
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I found this website: Alzheimer Research Forum; that is updated on a regular basis with the new and upcoming research of possible treatment avenues directed towards Alzheimer's Disease.
The latest research that was most intriguing is a possible "immunization" against the disease. The research was initially directed towards a specific genetic strain of mice who overproduce amyloid Beta and develop symptoms of Alzheimer's. Small amounts of amyloid beta were injected into young mice, resulting in antibody production, ultimately protecting against brain deterioration and learning deficits that the mice would have developed otherwise. It was found that people could also be induced to produce antibodies against amyloid beta. The therapy ended up producing life threatening side effects in some patients, therefore research was stopped.
Citation:
Antibodies against β-Amyloid Slow Cognitive Decline in Alzheimer's Disease
Christoph Hock et al.
Division of Psychiatry Research, University of Zurich, August Forel Strasse 1, 8008, Zurich, Switzerland
Received 26 March 2003; Revised 10 April 2003; accepted 30 April 2003 Published: May 21, 2003 Available online 17 April 2004.
Here is the abstract:
"To test whether antibodies against β-amyloid are effective in slowing progression of Alzheimer's disease, we assessed cognitive functions in 30 patients who received a prime and a booster immunization of aggregated Aβ42 over a 1 year period in a placebo-controlled, randomized trial. Twenty patients generated antibodies against β-amyloid, as determined by tissue amyloid plaque immunoreactivity assay. Patients who generated such antibodies showed significantly slower rates of decline of cognitive functions and activities of daily living, as indicated by the Mini Mental State Examination, the Disability Assessment for Dementia, and the Visual Paired Associates Test of delayed recall from the Wechsler Memory Scale, as compared to patients without such antibodies. These beneficial clinical effects were also present in two of three patients who had experienced transient episodes of immunization-related aseptic meningoencephalitis. Our results establish that antibodies against β-amyloid plaques can slow cognitive decline in patients with Alzheimer's disease."
Here is the link to the website and the latest update on this immunotherapy approach. The cited articles are listed however since they have only been published within the last two months I was not able to access the full article through pubmed.
http://www.alzforum.org/new/detail.asp?id=1795
Good article - I wonder if the mice, themselves, also experienced side effects once injected with the amyloid beta. It's interesting that mice and humans have similar homology, and that's why they are good model organisms for research testing; however, there are still discrepancies between species' reactions to certain substances. If only humans could produce antibodies that were only specific to plaque formation reduction and not other systems within the body.
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