Cerebellar atrophy in Alzheimer's disease—clinicopathological correlations

Morphometry of the cerebellum of 11 subjects who died in the severe, final stage of Alzheimer's disease (AD) and of five age-matched subjects without dementia revealed significant atrophy in the AD group, with a decrease in the volume of the molecular layer by 24% and of the granular layer by 2...

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Bibliographic Details
Published in:Brain research 1999-02, Vol.818 (1), p.41-50
Main Authors: Wegiel, Jerzy, Wisniewski, Henryk M., Dziewiatkowski, Jerzy, Badmajew, Eulalia, Tarnawski, Michal, Reisberg, Barry, Mlodzik, Bogdan, De Leon, Mony J., Miller, Douglas C.
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Alzheimer Disease - pathology
Alzheimer's disease
Atrophy
Biological and medical sciences
Case-Control Studies
Cerebellum
Cerebellum - pathology
Cerebral Amyloid Angiopathy - pathology
Cerebral Cortex - pathology
Clinicopathological correlation
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Female
Humans
Male
Medical sciences
Meninges - pathology
Morphometry
Neurology
Neuronal loss
Neurons - pathology
Purkinje Cells - pathology
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Summary:Morphometry of the cerebellum of 11 subjects who died in the severe, final stage of Alzheimer's disease (AD) and of five age-matched subjects without dementia revealed significant atrophy in the AD group, with a decrease in the volume of the molecular layer by 24% and of the granular layer by 22% in comparison with controls. The 32% decrease in the total number of Purkinje cells that was observed correlates with the atrophy of the molecular layer, whereas the 30% reduction in the total number of granule cells correlates with the atrophy of the molecular and granular layers. A unique pattern of Alzheimer-type pathology was observed in the cerebellum: (1) there were no neurofibrillary changes in the cerebellum of either the control or the AD subjects, (2) there was almost the same extent of leptomeningeal and cortical amyloid angiopathy in the normal aged subjects and in the AD patients, and (3) the presence of plaques was noted in the AD group, but not in the control group. This pattern of pathology suggests that two factors might be considered in the etiopathogenesis of cerebellar atrophy: (1) transneuronal degeneration and neuronal loss resulting from primary pathologic changes in cerebral structures and (2) parenchymal cerebellar ß-amyloidosis. The correlation between the temporal duration of AD and both the decrease of the total number of granule cells ( r=0.86, p
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(98)01279-7