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Cholinergic and Non-Cholinergic Neurotransmitter Hypotheses for Alzheimer’s Disease

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Alzheimer’s and Parkinson’s Disease

Part of the book series: Advances in Behavioral Biology ((ABBI,volume 29))

Abstract

Together with Parkinson’s disease, Alzheimer’s disease (AD) is one of a group of disorders that Gowers called abiotrophies [1], in which unexplained nerve cell loss appears to occur in selected areas (that is substantia nigra and cortex, respectively). During the last decade there has been considerable debate as to the importance and extent of neuronal loss in AD. The early studies of Kety, as well as recent in situ tomography [2] reveals some evidence for depressed brain energy metabolism. As we will show biochemical studies have made a contribution to these problems and give indications of the types of neurone and metabolic processes affected. Whenever possible we interpret changes in biochemical constituents in terms of their supposed cellular or subcellular identity and probable physiological action, although it is realized that this is an oversimplification, particularly for excitatory amino acid transmitters. A distinction has often been made between presenile and senile forms of AD but this division is not retained as similiar histological changes are seen in the cortex (neurofibrillary tangles within pyramidal neurones and senile or neuritic plaques in neuropil, composed of amyloid surrounded by fragments of enlarged axons and nerve terminals).

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© 1986 Plenum Press, New York

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Bowen, D.M., Francis, P.T., Palmer, A.M. (1986). Cholinergic and Non-Cholinergic Neurotransmitter Hypotheses for Alzheimer’s Disease. In: Fisher, A., Hanin, I., Lachman, C. (eds) Alzheimer’s and Parkinson’s Disease. Advances in Behavioral Biology, vol 29. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2179-8_7

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  • DOI: https://doi.org/10.1007/978-1-4613-2179-8_7

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-9283-8

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