QUANTITATIVE NEUROPATHOLOGIC ANALYSIS OF PICKS-DISEASE CASES - CORTICAL DISTRIBUTION OF PICK BODIES AND COEXISTENCE WITH ALZHEIMERS-DISEASE

Citation
Pr. Hof et al., QUANTITATIVE NEUROPATHOLOGIC ANALYSIS OF PICKS-DISEASE CASES - CORTICAL DISTRIBUTION OF PICK BODIES AND COEXISTENCE WITH ALZHEIMERS-DISEASE, Acta Neuropathologica, 87(2), 1994, pp. 115-124
Citations number
86
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00016322
Volume
87
Issue
2
Year of publication
1994
Pages
115 - 124
Database
ISI
SICI code
0001-6322(1994)87:2<115:QNAOPC>2.0.ZU;2-0
Abstract
Pick's disease is characterized morphologically by severe atrophy of t he frontal and temporal lobes and the presence in the cerebral cortex of degenerative neuronal lesions referred to as Pick bodies. In the pr esent study, we analyzed the regional and laminar distribution of Pick bodies in a series of 16 Pick's disease cases. These distribution and density patterns were compared with these observed for neurofibrillar y tangles in Alzheimer's disease. Very high densities of Pick bodies w ere observed Ammon's horn, subiculum, entorhinal cortex, and in the gr anule cell layer of the dentate gyrus. In the frontal and temporal neo cortex, they were preferentially distributed in layers II and VI. All of the Pick's disease cases also exhibited neurofibrillary tangles in the frontal and temporal areas and in the hippocampal formation, with higher densities in layers II-III than in layers V-VI of the neocortic al regions. Interestingly, this laminar distribution of neurofibrillar y tangles was strikingly different from that observed in Alzheimer's d isease cases, where they were more numerous in the infragranular layer s than in the supragranular layers. In addition, a few Pick's disease cases also had cortical senile plaques. These results suggest that the presence of neurofibrillary tangles in Pick's disease may be more fre quent than previously reported, and that Pick's disease and Alzheimer' s disease may coexist in certain cases. The lesion distribution patter ns suggest that different populations of cortical neurons are affected in Pick's and Alzheimer's diseases, and that alterations of select co rticocortical and corticosubcortical projections may distinguish these forms of dementia. It is also possible that these two disorders share certain pathogenetic mechanisms, even though both display specific pa tterns of regional and neuronal vulnerability to the degenerative proc esses.