Olfactory epithelium amyloid-β and paired helical filament-tau pathology in Alzheimer disease
Objective Olfactory dysfunction is common in Alzheimer disease (AD) and other neurodegenerative diseases. Paired helical filament (PHF)‐tau, α‐synuclein, and amyloid‐β lesions occur early and severely in cerebral regions of the olfactory system, and they have also been observed in olfactory epitheli...
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Published in | Annals of neurology Vol. 67; no. 4; pp. 462 - 469 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.04.2010
Wiley-Liss |
Subjects | |
Online Access | Get full text |
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Summary: | Objective
Olfactory dysfunction is common in Alzheimer disease (AD) and other neurodegenerative diseases. Paired helical filament (PHF)‐tau, α‐synuclein, and amyloid‐β lesions occur early and severely in cerebral regions of the olfactory system, and they have also been observed in olfactory epithelium (OE). However, their frequency, abundance, and disease specificity, and the relationships of OE pathology to brain pathology have not been established.
Methods
We investigated the pathological expression of amyloid‐β, PHFtau, α‐synuclein, and TDP‐43 in postmortem OE of 79 cases with AD, 63 cases with various other neurodegenerative diseases, and 45 neuropathologically normal cases.
Results
Amyloid‐β was present as punctate and small patchy aggregates in 71% of AD cases, compared with 22% of normal cases and 14% of cases with other diseases, and in greater amounts in AD than in either of the other 2 diagnostic categories. PHFtau was evident in dystrophic neurites in 55% of cases with AD, 34% with normal brains, and 39% with other neurodegenerative diseases, also at higher densities in AD. α‐Synuclein was present in dystrophic neurites in 7 cases, 6 of which also had cerebral Lewy bodies. Pathological TDP‐43 inclusions were not observed in the OE in any cases. Amyloid‐β and to a lesser degree, PHFtau ratings in OE significantly correlated with cortical Aβ and PHFtau lesion ratings in the brain.
Interpretation
These data demonstrate that AD pathology in the OE is present in the majority of cases with pathologically verified AD and correlates with brain pathology. Future work may assess the utility of amyloid‐β and PHFtau measurement in OE as a biomarker for AD. ANN NEUROL 2010;67:462–469 |
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Bibliography: | NIH - No. AG10124 ArticleID:ANA21910 ark:/67375/WNG-LXM51VZV-5 istex:B45DE674C18CC6083CA7CFA8FAA561E987EECC69 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0364-5134 1531-8249 |
DOI: | 10.1002/ana.21910 |