Alzheimer's Disease is characterized pathologically by two
principal hallmark lesions: the senile plaque and the
neurofibrillary tangle. Since the identification of each over 100
years ago, the major protein components have been elucidated. This
has led in turn to the elaboration of metabolic cascades involving
amyloid- production in the case of the senile plaque, and
phosphorylated-tau protein in the case of the neurofibrillary
tangle. The pathogenesis and histogenesis of each have been the
source of extensive investigation and some controversy in recent
years, as both cascades have been implicated in the pathogenesis of
Alzheimer's Disease, relied upon in the diagnostic criteria for
Alzheimer's Disease at autopsy, and targeted for therapeutic
intervention. With the accumulation of data and expansion of
knowledge of the molecular biology of Alzheimer's Disease, it
appears that the enthusiasm for successful intervention has been
premature. In this book, we detail the discovery and
characterization of the major pathological lesions, their
associated molecular biology, their relationship to clinical
disease, and potential fundamental errors in understanding that may
be leading scientific investigators in unintended directions. Table
of Contents: Introduction / Plaques / Neurofibrillary Degeneration
/ Complexities / Synopsis and Conclusion / References / Author
Biographies
General
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