Abstract
Alzheimer’s disease is characterized clinically by progressive and inevitable decline and loss of all higher cognitive functions over a period of years. This clinical decline is accompanied by the spread across cerebral cortical and subcortical regions of two salient neuropathological features: intraneuronal neurofibrillary tangles and complex neuritic β-amyloid-containing plaques (1,2). These plaques contain extracellular deposits of β-amyloid and a number of other proteins (3–6) as well as degenerating (dystrophic) neuritic processes and — importantly — activated glia elaborating a number of neurotrophic and immunomodulatory cytokines that drive and orchestrate the inception and evolution of these plaques (7–10). These cardinal neuropathological features are, in turn, accompanied by progressive neuronal loss and decreased density of synaptic elements within the cerebral cortical neuropil (11).
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Mrak, R.E., Griffin, W.S.T. (2001). Glial Cells in Alzheimer’s Disease. In: Molecular Mechanisms of Neurodegenerative Diseases. Contemporary Clinical Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-006-3_3
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