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Cortical Metabolism, Acetylcholinesterase Staining and Pathological Changes in Alzheimers Disease

Published online by Cambridge University Press:  18 September 2015

E.G. McGeer ,
P.L. McGeer ,
H. Kamo ,
H. Tago  and
R. Harrop
E.G. McGeer*
Affiliation:
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia and Department of Mathematics, Simon Fraser University, Vancouver
P.L. McGeer
Affiliation:
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia and Department of Mathematics, Simon Fraser University, Vancouver
H. Kamo
Affiliation:
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia and Department of Mathematics, Simon Fraser University, Vancouver
H. Tago
Affiliation:
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia and Department of Mathematics, Simon Fraser University, Vancouver
R. Harrop
Affiliation:
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia and Department of Mathematics, Simon Fraser University, Vancouver
*
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., Canada V6T 1W5
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Abstract:

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The local cerebral metabolic rate for glucose (LCMRgl) was determined by positron emission tomography (PET) using the 18F-fluorodeoxyglucose method in a series of Alzheimer patients and normal controls. The LCMRgl declined in the cerebral cortex with age, but the decrement was significantly greater in the clinically diagnosed Alzheimer's cases. Comparison of PET and psychological data indicated that, as the disease progressed clinically, the reduction in cortical LCMRgl and the number of cortical regions involved also increased. Variable regions of cortex were involved in the early stages but the temporal, parietal and frontal regions were most typically affected. One case coming to autopsy showed that the severity of the LCMRgl decline paralleled loss of neurons in the cortex and their replacement with astroglia.

A case of Pick's disease coming to autopsy had shown a different and highly characteristic pattern of cortical metabolic defect. In this case also a poor metabolic rate was associated with extensive gliosis.

Acetylcholinesterase (AChE) staining of the cerebral cortex in elderly normals and Alzheimer's disease cases with a new, highly sensitive method showed that in Alzheimer's disease there was an extensive loss of AChE-positive fibers with senile plaques frequently incorporating AChE-positive fiber debris. AChE staining of the substantia innominata area, where the cells giving rise to these neocortical fibers are presumably located, also showed evidence of degenerating cells and fibers.

Type
Biochemical Studies
Information
Canadian Journal of Neurological Sciences , Volume 13 , Issue S4 , November 1986 , pp. 511 - 516
Copyright
Copyright © Canadian Neurological Sciences Federation 1986

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