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Alzheimer’s Disease and Animal Models

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Molecular Mechanisms of Aging

Abstract

Alzheimer’s disease (AD), the most common type of age-associated dementia, is characterized by progressive impairments in memory, cognition, language, praxis, visual-spatial skills, and behavior (McKhann et al., 1984; Khachaturian, 1985). These abnormalities are due to involvement of certain neuronal circuits in several regions of brain, including systems within amydala, hippocampus, neocortex, basal forebrain, and brainstem. For example, in virtually every case, AD affects basal forebrain cholinergic neurons, which express receptors for nerve growth factor (NGF). Perikarya of many neurons in involved systems develop neurofibrillary tangles (NFT) (fibrillar intracytoplasmic inclusions) and abnormally enlarged distal axons/terminals (forming neurites that surround senile plaques). Amyloid, deposited in plaques and around blood vessels (congophilic angiopathy), is made up of a 4-kiloDalton (kD) β/A4 peptide, derived from the amyloid precursor protein (APP). This brief review focuses on: the neuropathology of AD; investigations of the pathogenesis of age-associated abnormalities in the brains of aged nonhuman primates; and studies of the effects of NGF on experimentally induced degenerative changes in basal forebrain cholinergic neurons of animals.

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© 1990 Springer-Verlag Berlin Heidelberg

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Price, D.L., Martin, L.J., Koo, E.H., Sisodia, S.S., Koliatsos, V.E., Cork, L.C. (1990). Alzheimer’s Disease and Animal Models. In: Beyreuther, K., Schettler, G. (eds) Molecular Mechanisms of Aging. Veröffentlichungen aus der Geomedizinischen Forschungsstelle der Heidelberger Akademie der Wissenschaften, vol 1990 / 1990/2. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84224-5_15

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  • DOI: https://doi.org/10.1007/978-3-642-84224-5_15

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