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Arch Neurol. 2001 Nov;58(11):1817-20.

Alpha-synuclein in familial Alzheimer disease: epitope mapping parallels dementia with Lewy bodies and Parkinson disease.

Author information

  • 1Department of Neurology, Medical College of Pennsylvania--Hahnemann University, 3300 Henry Ave, Philadelphia, PA 19129, USA. carol.lippa@drexel.edu

Abstract

BACKGROUND:

Alpha-synuclein is a major component of Lewy bodies (LBs) in Parkinson disease and dementia with LBs and of glial cytoplasmic inclusions in multiple system atrophy. However, epitope mapping for alpha-synuclein is distinctive in different neurodegenerative diseases. The reasons for this are poorly understood but may reflect fundamental differences in disease mechanisms.

OBJECTIVE:

To investigate the alpha-synuclein epitope mapping properties of LBs in familial Alzheimer disease.

DESIGN AND SETTING:

We compared LBs in familial Alzheimer disease with those in synucleinopathies by probing 6 brains of persons with familial Alzheimer disease using a panel of antibodies to epitopes spanning the alpha-synuclein protein. Results were compared with data from brains of persons with Parkinson disease, dementia with LBs, and multiple system atrophy.

RESULTS:

The brains of persons with familial Alzheimer disease showed consistent staining of LBs with all antibodies, similar to Parkinson disease and dementia with LBs but different from alpha-synuclein aggregates that occurred in multiple system atrophy.

CONCLUSIONS:

These data suggest that the epitope profiles of alpha-synuclein in LBs are similar, regardless of whether the biological trigger is related to synuclein or a different genetic pathway. These findings support the hypothesis that the mechanism of alpha-synuclein aggregation is the same within cell types but distinctive between cell types.

PMID:
11708989
[PubMed - indexed for MEDLINE]
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