Abstract
The distinguishing pathological hallmark of Alzheimer’s disease (AD) is the presence of proteinaceous deposits, referred to as senile plaques, within the higher learning centers of the brain (1). These plaques are comprised predominantly of multimeric fibrils of the amyloid β (Aβ) peptide (2), a 40–43 amino acid long proteolytic fragment that is cleaved from the larger amyloid precursor protein (APP) (3). Genetic data suggest that senile plaques are key causative agents in AD, as all known mutations that cause early-onset familial AD (4–8) result in an increased production of the amyloidogenic Aβ1–42 isoform (9–13). Although the deposition of multimeric Aβ fibrils into plaques is likely to be a requisite step in AD onset, there is still uncertainty as to how Aβ and neuritic plaques might cause the neuropathology that leads to the characteristic dementia of this disease. One compelling hypothesis that is supported by substantial experimental data postulates that senile plaques cause glial cell activation, resulting in the release of a host of glial-derived molecules that contribute to disease progression.
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Brunden, K.R., Frederickson, R.C.A. (2002). Activated Neuroglia in Alzheimer’s Disease. In: de Vellis, J.S. (eds) Neuroglia in the Aging Brain. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-105-3_20
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