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- W71492373 abstract "Alzheimer’s disease (AD) represents the most common form of dementia in elderly individuals, affecting nearly 11% of the population over 65 years of age. Possibly up to 50% of those over 85 can be diagnosed clinically as having “probable AD” (Moss and Albert, 1988; Evans et al., 1992). Clinical and neuropathological studies also indicate that cases with AD alone or in combination with other diseases account for more than 50% of all demented patients over 65 (Tomlinson et al., 1968; Mortimer et al., 1981; Fallet-Bianco et al., 1990; Jorm, 1991; Copeland et al., 1992; Fratiglioni et al., 1991). Our understanding of the structural, molecular, and biochemical nature of AD has grown substantially in recent years, yet the causal pathogenetic events that lead to dementia are not known. Many hypotheses on the development of the typical lesions of AD have been proposed and, despite a considerable diversity of data, it appears that the structural and functional changes seen in AD isolate the cerebral cortex as the predominant substratum of the clinical symptomatology observed in demented patients (De Lacoste and White, 1993; Morrison, 1993; Hof and Morrison, 1994, 1996; Hof et al., 1995a; Hof, 1997). When considering the pathology at regional and cellular levels, however, a generalized loss of cortical function appears unlikely, as AD involves certain populations of neurons displaying a specific regional and laminar distribution and specific connectivity patterns, whereas other neuron types remain largely unaffected (Morrison et al., 1987; Morrison, 1993; Hof and Morrison, 1994, 1996; Hof et al., 1995a; Gómez-Isla et al., 1996, 1997; Bobinski et al., 1997; Hof, 1997; Morrison and Hof, 1997). Thus, different degrees of neuronal vulnerability exist in AD that may be described in terms of morphologic and biochemical characteristics among distinct neuronal populations and sets of connections. In addition, the study of pathologic alterations associated with normal brain aging may offer clues as to the cellular mechanisms responsible for the development of dementia, because many neuronal populations that are devastated in early AD undergo mild but consistent changes in cognitively intact elderly individuals as well." @default.
- W71492373 created "2016-06-24" @default.
- W71492373 creator A5045886993 @default.
- W71492373 creator A5053754870 @default.
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- W71492373 date "1999-01-01" @default.
- W71492373 modified "2023-10-12" @default.
- W71492373 title "Cortical Neuropathology in Aging and Dementing Disorders" @default.
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