Book contents
- Frontmatter
- Contents
- Contributors
- Foreword
- Acknowledgements
- Biographical note on F. H. Lewy
- Abbreviations
- Group photograph
- Introduction
- Part one Clinical issues
- Part two Pathological issues
- 15 Pathological significance of Lewy bodies in dementia
- 16 Tautological tangles in neuropathologic criteria for dementias associated with Lewy bodies
- 17 What is the neuropathological basis of dementia associated with Lewy bodies?
- 18 Cytoskeletal and Alzheimer-type pathology in Lewy body disease
- 19 Diffuse Lewy body disease within the spectrum of Lewy body disease
- 20 Temporal lobe immunohistochemical pathology for tangles, plaques and Lewy bodies in diffuse Lewy body disease, Parkinson's disease, and senile dementia of Alzheimer type
- 21 Pathological and clinical features of Parkinson's disease with and without dementia
- 22 Dementia with Lewy bodies: relationships to Parkinson's and Alzheimer's diseases
- 23 What do Lewy bodies tell us about dementia and parkinsonism?
- 24 Pathogenesis of the Lewy body
- 25 Altered tau processing: its role in development of dementia in Alzheimer's disease and Lewy body disease
- 26 Cytoskeletal pathology in Alzheimer's disease and Lewy body dementia – an epiphenomenon?
- 27 Genetic correlations in Lewy body disease
- Résumeacute; of pathological workshop sessions
- Part three Treatment issues
- Appendices
- Index
- Plate section
23 - What do Lewy bodies tell us about dementia and parkinsonism?
from Part two - Pathological issues
Published online by Cambridge University Press: 06 July 2010
- Frontmatter
- Contents
- Contributors
- Foreword
- Acknowledgements
- Biographical note on F. H. Lewy
- Abbreviations
- Group photograph
- Introduction
- Part one Clinical issues
- Part two Pathological issues
- 15 Pathological significance of Lewy bodies in dementia
- 16 Tautological tangles in neuropathologic criteria for dementias associated with Lewy bodies
- 17 What is the neuropathological basis of dementia associated with Lewy bodies?
- 18 Cytoskeletal and Alzheimer-type pathology in Lewy body disease
- 19 Diffuse Lewy body disease within the spectrum of Lewy body disease
- 20 Temporal lobe immunohistochemical pathology for tangles, plaques and Lewy bodies in diffuse Lewy body disease, Parkinson's disease, and senile dementia of Alzheimer type
- 21 Pathological and clinical features of Parkinson's disease with and without dementia
- 22 Dementia with Lewy bodies: relationships to Parkinson's and Alzheimer's diseases
- 23 What do Lewy bodies tell us about dementia and parkinsonism?
- 24 Pathogenesis of the Lewy body
- 25 Altered tau processing: its role in development of dementia in Alzheimer's disease and Lewy body disease
- 26 Cytoskeletal pathology in Alzheimer's disease and Lewy body dementia – an epiphenomenon?
- 27 Genetic correlations in Lewy body disease
- Résumeacute; of pathological workshop sessions
- Part three Treatment issues
- Appendices
- Index
- Plate section
Summary
Summary
Lewy bodies remain an enigma. Their presence in the substantia nigra is often taken as a diagnostic criterion for idiopathic parkinsonism (IP, Parkinson's disease). Yet the first report of Lewy bodies in IP is an account of their appearance in the dorsal motor nucleus of the vagus, and the nucleus basalis of Meynert. More serious problems have arisen in recent years, partly as a result of improved techniques for detecting Lewy bodies. The more they have been looked for, the more they have been found. A further complicating factor is that they have different appearances in different regions of the brain. We know that Lewy bodies are made up from cytoskeletal products and they are associated with the death of neurons. They may contribute to the mechanism driving cell death. Alternatively, their formation may represent a compensatory adjustment in an attempt to ameliorate the demise of neurons. They have not helped us in an attempt to find the aetiology of IP, because they occur in such widely diverse settings as hereditary neurodegeneration (e.g. Hallervorden-Spatz disease) and viral infection (e.g. subacute sclerosing panencephalitis). Thus our knowledge, and our ignorance, concerning Lewy bodies leaves us in a tantalizing situation. Surely they are important clues to neurodegeneration, but as yet we have not been able to reveal the secrets that they should provide to help us unravel the pathogenesis of IP.
Introduction
James Parkinson described the clinical features of the disorder that bears his name in 1817 (Parkinson, 1817). In 1912, Lewy demonstrated the existence of neuronal inclusion bodies in the dorsal motor nucleus of the vagus and nucleus basalis of Meynert in Parkinson's disease.
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- Dementia with Lewy BodiesClinical, Pathological, and Treatment Issues, pp. 287 - 301Publisher: Cambridge University PressPrint publication year: 1996
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