scholarly journals Glucose metabolic rate and progression of illness in Alzheimer's disease

1995 ◽  
Vol 10 (8) ◽  
pp. 659-667 ◽  
Author(s):  
Benjamin V. Siegel ◽  
Monte S. Buchsbaum ◽  
Arnold Starr ◽  
Richard C. Mohs ◽  
Dirceu C. Neto
2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Paul Edison ◽  
Sanara Raza ◽  
Grazia Daniela Femminella ◽  
Eleanor G Blunt ◽  
Stefan Carver ◽  
...  

1996 ◽  
Vol 39 (7) ◽  
pp. 660
Author(s):  
L. Shihabuddin ◽  
M.S. Buchsbaum ◽  
P. Harvey ◽  
E. Hazlett ◽  
M. Haznedar ◽  
...  

1997 ◽  
Vol 37 (1) ◽  
pp. 10-19 ◽  
Author(s):  
Dan J. Stein ◽  
Monte S. Buchsbaum ◽  
Patrick R. Hof ◽  
Benjamin V. Siegel Jr. ◽  
Lina Shihabuddin

1996 ◽  
Vol 44 (10) ◽  
pp. 1232-1234 ◽  
Author(s):  
Kendall E Donaldson ◽  
William H Carpenter ◽  
Michael J. Toth ◽  
Michael I. Goran ◽  
Paul Newhouse ◽  
...  

Author(s):  
E.G. McGeer ◽  
P.L. McGeer ◽  
H. Kamo ◽  
H. Tago ◽  
R. Harrop

Abstract: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.


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