Alzheimer's Disease and IL1-BAPP interactions

A number of studies suggest that preventing the activation of microglia (and inflammatory cell infiltration in general) reduces the extent of neurological damage (in fact, I read a brand new study from the Nov. 9 Journal of Clinical Investigation found here http://www.ajc.com/health/content/shared-auto/healthnews/alzh/632918.html to reiiterate). Such has been the case in studies of experimental Alheimer’s, Parkinson’s, stroke, and multiple sclerosis (etc). We have discussed in great detail the immune responses and cell-to-cell interactions as they pertain to neurodegenerative diseases, particularly Alzheimer’s disease.
Microglia have long been thought of as the brain’s resident immune cell, similarly to macrophages and monocytes. Once stimulated in response to neurodegenerative events (whether it be aging or blunt trauma), microglia release a variety of proinflammatory mediators such as cytokines, free radicals, Nitric oxide, etc, all of which contribute to neuronal dysfunction and cell death, ultimately creating a vicious cycle. At the heart of that cycle is Interleukin 1. Many studies have shown IL-1 works in an autocrine and paracrine manner to further the progression of Alzheimer’s disease.
In the paracrine pathway, chronic overexpression of IL-1 reaches the periphery and overexpresses Beta Amyloid Precursor Protein and astrocytic S100B. This leads to the intrigue, because the brain of an alzheimer’s diseased patient shows severe brain volume reduction and degeneration of neurons and synapses. The degeneration is attributed to two characteristic lesions: extracellular deposits of Beta Amyloid peptide and the intracellular neurofibrillary tangles of the tau protein. Evidence linking IL-1 and B-APP is well documented (Griffin 1998), but what has not been completely understood is whether IL-1 is activating other cells to clean up the senile plaques, or if IL-1 furthers the progression of senile plaques. The Mayo clinic released an article declaring that Inflammation works to play a protective role during the progression of Alzheimer’s, which calls into question our current understanding of how cytokines are involved with B-APP (the obvious link to the formation of senile plaques) and quite possibly the future of treatment for Alzheimer’s Disease.