THE 1990’S the “amyloid hypothesis” for the cause of Alzheimer’s became the hot exciting new reason for the cause of Alzheimer’s disease. the idea is that beta-amyloid proteins build up to form plaques that damage brain cells. The brain plaque theory caught on like gangbusters and quickly became the conventional wisdom of the time. I’m writing this in 2019 and this theory is still prevalent as I’m scheduled to have another MRI this week called the PEC which shows the Doctors in what part of my brain the amyloid protein is present. It takes about an hour and a half because the shoot me full of a dye and then due an extensive MRI of my brain. Sounds wonderful doesn’t it.
This PEC test is one of the main reason my Doctor wanted me to get into this clinical study. From what she say’s the test is very expensive, not covered by Medicare and crucial to them understand what going on in my brain. Anyway it’s one of the main requirements of acceptance into the clinical trial I’m in. So I hope they find out great stuff from the test! After the test I’m supposed to start receiving the medicine or the placebo. I sure hope it’s the medicine -21/2 years on the placebo sure sounds like a wast to me.
simply Said: Amyloid plaques are clumps of a protein called beta amyloid. This plaque builds up around the cells in the brain that communicate or talk with each other. Amyloid beta is always a feature of Alzheimer’s disease, but. Amyloid plaques affect sensory & motor areas of the cerebral cortex as well as association areas, but NFTs are restricted to association areas.
Alzheimer’s illness is a dynamic dementia with loss of neurons and the nearness of two fundamental infinitesimal neuropathological trademarks: extracellular amyloid plaques and intracellular neurofibrillary tangles. Early onset AD, an uncommon familial shape, is caused because of change of one out of three qualities: (amyloid antecedent protein), (presenilin 2) or (presenilin 1). Sporadic shape happens more often than not after age of 65 and records for most cases; it in all likelihood comes about because of a blend of hereditary and impact of condition. Affirmed chance elements for sporadic AD are age and the nearness of the E4 allele of (Apolipoprotein E). Amyloid plaques contain for the most part of the neurotoxic peptide amyloid (A?, Abeta), cut consecutively from a bigger antecedent protein (APP) by two chemicals: ?-secretase (additionally called BACE1) and ?-secretase (involving four proteins, presenilin is one of them).
Amyloid Plaques and Neurofibrillary tangles(NTFs)
the moderate stage of Alzheimer’s, amyloid plaques and neurofibrillary tangles gradually extend into the area’s of the brain involved in recognising one’s body separately from the objects around it, as well as the parts involved in using language. That is why people begin to have problems not only in their daily tasks, but also in their social and work lives, which suffer a lot from the deterioration of their language abilities. For people in this stage of Alzheimer’s, the slightest conversation becomes extremely hard work. They lose the thread of their conversation and can no longer find the words to express themselves, and do not understand clearly when things are explained to them. At this same time, they also stop reading and writing which I am definitely not looking forward too. I love to read and write as I’ve told you. I write at least one blog post a day if not more. I asked my Doctor “When this will start to take place” and in her usually wisdom said she didn’t know. Neurologist’s favorite words are I Don’t know.
Despite the wide-spread blaming of cholesterol for Alzheimer’s disease and the widespread claiming of statins as a possible cure, none of these turn out to be true. The manufactures of statins have tried to claim that statins are a cure all for just about any human condition. Any claim made by a manufacturer of Statins I would take with a grain of salt The amyloid hypothesis therefor remains highly questionable and unconfirmed; cholesterol’s relationship to amyloid levels is inconclusive; high cholesterol is not a true risk factor for Alzheimer’s; and, statins do not appear to inhibit amyloid plaques at reasonable doses and can even cause neuronal cell death at high doses.