Abstract
Alzheimer’s disease (AD) is characterized clinically by memory deficits and progressive cognitive decline leading to incapacitating dementia and death. Gross examination of the AD brain indicates that the cerebral cortex is most severely affected, with notable atrophy of the medial temporal lobe, temporal pole (including the subcortical amygdala), midfrontal, and orbitofrontal cortex. Pathologically, the disease is characterized by the deposition of filamentous material in intracellular and extracellular compartments in the form of neurofibrillary tangles (NFTs), neuropil threads (NTs), and senile plaques (SPs), predominantly within the hippocampal formation (entorhinal cortex, Amnion’s horn—CA1, CA2, CA3, and CA4—dentate gyrus, and subicular complex) and neocortex (the secondary association and polymodal cortex). Additionally, subsets of neurons appear selectively vulnerable to neurodegeneration within the AD brain, including GA1 pyramidal neurons of the hippocampal formation and layers II, III, and V corticocortical projection neurons of secondary association cortex, leading to regionally specific synaptic and connectivity-based degeneration (see Hof et al., this volume). A diagnosis of AD is made postmortem on aged patients who display progressive cognitive decline and the presence of abundant NFTs and SPs with dystrophic processes—the so-called neuritic plaque—upon microscopic evaluation of hippocampus and neocortex.
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Ginsberg, S.D., Schmidt, M.L., Crino, P.B., Eberwine, J.H., Lee, V.MY., Trojanowski, J.Q. (1999). Molecular Pathology of Alzheimer’s Disease and Related Disorders. In: Peters, A., Morrison, J.H. (eds) Cerebral Cortex. Cerebral Cortex, vol 14. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4885-0_17
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