The Elimination of Cytotoxic Senile Plaques in Alzheimer’s Disease Using Stem Cell Therapy

It is known that the laying down of the amyloid protein outside the nerve cells is one factor contributing to the onset of Alzheimer’s disease, as this protein basically acts to form neuritic – cytotoxic – plaques, which begins the pathological process which leads to Alzheimer’s disease. It is known that in later stage Alzheimer’s disease, abnormal protein filaments – formed from tau proteins – also appear in the neurons in the brain, which normally act to stabilize the microtubules but in this case, due to the formation of paired helical filaments, destabilizes the system.
What are the causes of the disease There are currently three major hypotheses put forward to explain how the disease is caused, one of which, the cholinergic hypothesis argues that acetylcholine deficiency, through a deficiency in its production, is responsible for the deterioration seen, as acetylcholine is normally responsible for transmitting information in the neurons. This hypothesis has generally been dismissed by the research community, however, as treatment with acetylcholinesterase, the enzymes that break down acetylcholine, in order to stop the loss of acetylcholine, have been found to be ineffective.
Other researchers have concentrated on the tau-proteins, as it is believed that abnormalities in the tau proteins lead to the symptoms seen in Alzheimer’s disease, whereas others concentrate on the formation of beta-amyloid deposits, as a major cause of Alzheimer’s disease. It is noted, however, even by researchers working on understanding these two possible causal pathways, that the presence of cytotoxic plaques or protein tangles does not per se explain the onset of Alzheimer’s disease, and so many researchers, whilst concentrating on these research avenues, keep an open mind as to the possible causes of Alzheimer’s disease.&nbsp.&nbsp.