Serveur d'exploration sur la maladie de Parkinson

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Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex

Identifieur interne : 002781 ( Main/Exploration ); précédent : 002780; suivant : 002782

Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex

Auteurs : H. Braak [Allemagne] ; E. Braak [Allemagne]

Source :

RBID : ISTEX:CBA8AB4A8F8BFD97C8C3C64C3B1428A0D2885D1E

Abstract

Summary: Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.

Url:
DOI: 10.1007/BF02251245


Affiliations:


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<title level="j">Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title>
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<div type="abstract" xml:lang="en">Summary: Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.</div>
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