Molecular forms of acetylcholinesterases in Alzheimer's disease

S. G. Younkin, B. Goodridge, Mindy Joy Katz, G. Lockett, D. Nafziger, M. F. Usiak

Research output: Contribution to journalArticle

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Abstract

In this study, we examined 26 cases of Alzheimer's disease (AD) and 14 age-matched controls. In Brodmann area 21 cerebral cortex of the AD cases, there was no change in soluble G1 and G4 acetylcholinesterase (AChE) (EC 3.1.1.7), a significant 40% decrease in membrane-associated G4 AChE, significant 342 and 406% increases in A12 and A8 AChE, and a significant 71% decrease in choline acetyltransferase (ChAT) (EC 2.3.1.6). Our working hypothesis to account for these changes postulates 1) that soluble globular forms are unchanged because they are primarily associated with intrinsic cortical neurons that are relatively unaffected by AD, 2) that ChAT and membrane-associated G4 AChE decrease because they are primarily associated with incoming axons of cholinergic neurons that are abnormal in AD, and 3) that asymmetric forms of AChE increase because of an acrylamide-type impairment of fast axonal transport in diseased incoming cholinergic axons. In the nucleus basalis of Meynert (nbM) of the 26 AD cases, there was a significant 61% decrease in the number of cholinergic neurons, an insignificant 23% decrease in nbM ChAT, a significant 298% increase in nbM ChAT per cholinergic neuron, and a significant 7% increase in the area of cholinergic perikarya. To account for the increased ChAT in cholinergic neurons and the enlargement of cholinergic perikarya, we propose that slow axonal transport may be impaired in nbM cholinergic neurons in AD.

Original languageEnglish (US)
Pages (from-to)2982-2988
Number of pages7
JournalFederation Proceedings
Volume45
Issue number13
StatePublished - 1986
Externally publishedYes

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Choline O-Acetyltransferase
Acetylcholinesterase
Cholinergic Neurons
Basal Nucleus of Meynert
Alzheimer Disease
Cholinergic Agents
Axonal Transport
Axons
compound A 12
Membranes
Acrylamide
Cerebral Cortex
Neurons

ASJC Scopus subject areas

  • Medicine(all)

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Younkin, S. G., Goodridge, B., Katz, M. J., Lockett, G., Nafziger, D., & Usiak, M. F. (1986). Molecular forms of acetylcholinesterases in Alzheimer's disease. Federation Proceedings, 45(13), 2982-2988.

Molecular forms of acetylcholinesterases in Alzheimer's disease. / Younkin, S. G.; Goodridge, B.; Katz, Mindy Joy; Lockett, G.; Nafziger, D.; Usiak, M. F.

In: Federation Proceedings, Vol. 45, No. 13, 1986, p. 2982-2988.

Research output: Contribution to journalArticle

Younkin, SG, Goodridge, B, Katz, MJ, Lockett, G, Nafziger, D & Usiak, MF 1986, 'Molecular forms of acetylcholinesterases in Alzheimer's disease', Federation Proceedings, vol. 45, no. 13, pp. 2982-2988.
Younkin SG, Goodridge B, Katz MJ, Lockett G, Nafziger D, Usiak MF. Molecular forms of acetylcholinesterases in Alzheimer's disease. Federation Proceedings. 1986;45(13):2982-2988.
Younkin, S. G. ; Goodridge, B. ; Katz, Mindy Joy ; Lockett, G. ; Nafziger, D. ; Usiak, M. F. / Molecular forms of acetylcholinesterases in Alzheimer's disease. In: Federation Proceedings. 1986 ; Vol. 45, No. 13. pp. 2982-2988.
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