Abstract
Investigations concerning the pathogenesis of Alzheimer’s disease initially focused on neurotransmitters, enzymes involved in their synthesis and their neuronal receptors. It eventually became apparent that abnormalities in neurotransmitter systems were probably not the cause of Alzheimer’s disease, but rather the result of it, i.e. dead or dying neurons failed to synthesize the neurotransmitters and receptors found to be depleted in this disease. Since the major pathological findings in Alzheimer’s disease are neuronal loss, neurofibrillary tangles, senile plaques and cerebrovascular amyloidosis, a major emphasis on delineating the nature of these lesions appeared to offer an approach to the understanding of the nature of this disease. These studies employing protein chemistry have resulted in new pathologic concepts and the introduction of molecular biology in the deciphering of the pathogenesis of Alzheimer’s disease.
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Glenner, G.G. (1990). Proteins and Proteolysis in the Pathogenesis of Alzheimer’s Disease. In: Nagatsu, T., Fisher, A., Yoshida, M. (eds) Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 38A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5844-2_5
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DOI: https://doi.org/10.1007/978-1-4684-5844-2_5
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