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EDITORIAL |
| Cortical lewy body disease |
Correspondence to:
Correspondence to:
Dr David J Burn
Department of Neurology, Regional Neurosciences Centre, Newcastle General Hospital, University of Newcastle upon Tyne NE4 6BE, UK; djburn@ncl.ac.uk
Keywords: Lewy body; dementia; Parkinsons disease
Abbreviations: CERAD, consortium to establish a registry for Alzheimers disease; CLB, cortical Lewy bodies; DLB, dementia with Lewy bodies; NFT, neurofibrillary tangle; NIA, National Institute on Aging; PDD, Parkinsons disease with dementia
| The first 150 words of the full text of this article appear below. |
Cortical Lewy body disease is a pathological observation rather than a distinct clinicopathological entity. Cortical Lewy bodies (CLB) are typically found in Parkinsons disease and dementia with Lewy bodies (DLB), although they may also occur in other neurological disorders. Unlike their brain stem counterparts, CLB are less distinctive and are poorly visualised using conventional histochemical methods. The protein
-synuclein is the main component of Lewy bodies and the related dystrophic Lewy neurites1; immunohistochemistry using antibodies raised against this protein has greater sensitivity in demonstrating Lewy pathology within the cerebral cortex than histochemical methods and anti-ubiquitin immunohistochemistry.
Dementia is a common occurrence in Parkinsons disease, with a prevalence of 2040% in cross sectional studies,2,3 but a cumulative incidence approaching 80%.4 The clinical phenotype of this dementia shares many features with DLB. In neither condition, however, has the relation between the presence of CLB and the dementing
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M. L. Kramer and W. J. Schulz-Schaeffer Presynaptic {alpha}-Synuclein Aggregates, Not Lewy Bodies, Cause Neurodegeneration in Dementia with Lewy Bodies J. Neurosci., February 7, 2007; 27(6): 1405 - 1410. [Abstract] [Full Text] [PDF] |
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