Anatomy of Pathological Alterations in Alzheimer’s Disease

Abstract

Even by inspection of the gross brain, it is evident that Alzheimer’s disease (AD) neuropathological changes do not occur randomly or uniformly, but instead target the medial temporal lobe and association cortices of the temporal and parietal areas (1–3). It might be expected, given the complex topography of brain architecture, that on finer examination, this distribution would show a pattern of vulnerability definable at the level of neural systems, cytoarchitectural fields, and even specific lamina within cytoarchitectural fields. Our anatomical studies of AD neuropathology have shown that this is indeed the case. Neurofibrillary tangles (NFT), senile plaques (SP), and neuronal loss affect individual cytoarchitectural areas and laminae in an extraordinarily specific and selective manner. Based on application of neuroanatomical principles and extrapolation of connectional data from the nonhuman primate experimental system, we have suggested that these lesions destroy major feed-forward and feedback projections, leading to disruption of neural systems related to memory and cognition (4). In this chapter, I will briefly review the major themes of the anatomical alterations in AD from the perspective of the studies we have carried out over the last decade.KeywordsDown SyndromeEntorhinal CortexNeurofibrillary TangleSenile PlaqueAssociation CortexThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.