Until just a couple of weeks ago, the accepted cause of the dreaded disease was plaque-like deposits found in the brain of those suffering from the malady. Scientists at University of California in Los Angeles and Northwestern University in Evanston Il. state that their findings can open a whole new direction of research leading to new treatments or possibly a cure.
The findings, published in the most recent issue of "Trends in Neurosciences", still considers the molecule called Beta-Amyloid as the principal culprit. (Amyloids are hard, waxy deposits consisting of protein & polysacchrides that are the end product of tissue degeneration.) The actual origins (basic cause) of the disease, however, is now attributed to the formation of toxic proteins rather than to the build-up of plaque and tangles within the cells of the brain.
Alzheimer's Disease, starts with memory loss and progresses at varying speeds to profound dementia and eventual death. The ailment afflicts approximately 4 million Americans today. There are a few medications on the open market that can slow that progression, but there is no stopping it.
In an interview granted to Reuters News Service, Dr. Caleb Finch, director of the Neurogerontology Division at the University of Southern California Andrus Center's Gerontology Research Institute, "We were able to identify, in laboratory test tubes, a new kind of toxic activity that is implicated as a root cause of Alzheimer's."
What the researchers discovered was a unique form of a wadded-up amyloid called amyloid b-derived diffusible ligands they named ADDL's. Addl's form in the presence of certain inflammatory proteins in the brain. These entities have chemical and toxicological properties very different from the single beta-amyloid molecules and clumps of them that have joined into fibrils.
It must be noted that for several years, Alzheimer's research has focused on ways to prevent the formation of the fibrils which, in turn, coalesce to form plaques in the brain. These plaques have been shown to cause nerve cell damage and death.
Another characteristic of ADDLs (unlike fibrils) is that they are highly selective in their toxicity. Research has demonstrated that ADDLs affect only the cells that have been found to atrophy in Alzheimer's. Fibrils, on the other hand, kill a wide range of cells including cell types that could remain healthy until the moment of the patient's death.
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