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
25 - Altered tau processing: its role in development of dementia in Alzheimer's disease and Lewy body disease
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
Altered processing of tau protein is a characteristic feature of Alzheimer's disease (AD) that, unlike the accumulation of amyloid β-protein, is strongly correlated with clinical dementia. In AD, tau is substantially redistributed from its soluble, predominantly axonal form into insoluble PHF-tau that accumulates in the somatodendritic compartment. Although hyperphosphorylated tau also accumulates, this accounts for no more than 5% of the total PHF-tau during any stage of the development of AD. In contrast, cortical Lewy body dementia in the elderly is not associated with these changes in tau processing and such patients have less than one-tenth of the levels of both PHF-tau and neurofibrillary pathology as those found in AD. These findings support the notion that the pathobiology of these two disorders is distinct and provide the opportunity to compare non-PHF- with PHF-type dementias. Both these late-onset dementias are associated with comparable increases in the frequency of the apolipoprotein E (APO E) type ∈4 allele (in excess of 30%, as compared with 14% in controls and 10% in Parkinson's disease). The extent of abnormal PHF-tau levels in AD is unaffected by the presence of an e4 allele, suggesting that APO E polymorphisms do not directly influence the pathological processing of tau. These findings suggest that cortical Lewy body dementia has an aetiopathogenesis that is distinct from AD. Furthermore, APO E polymorphisms influence the development of dementia in both AD and cortical, but not subcortical Lewy body disease by mechanisms(s) that remain to be identified.
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- Information
- Dementia with Lewy BodiesClinical, Pathological, and Treatment Issues, pp. 308 - 323Publisher: Cambridge University PressPrint publication year: 1996