Dystrophic neurites are associated with early stage extracellular neurofibrillary tangles in the parkinsonism-dementia complex of Guam |
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Authors: | Claudia Schwab John C Steele P L McGeer |
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Institution: | (1) Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C. V6T 1Z3, Canada Tel.: 1-604-822-7377; Fax: 1-604-822-7086, CA;(2) Guam Memorial Hospital, Agana, Guam, USA, GU |
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Abstract: | We found tangle-associated neuritic clusters (TANCs), previously reported as being present in Alzheimer’s disease (AD), to
be common in early and mild cases of the parkinsonism-dementia complex of Guam (PDC, bodig disease). These entities were observed
around extracellular neurofibrillary tangles (eNFTs), apparently as a transient phenomenon. They were not observed around
normal neurons, or neurons with intracellular neurofibrillary tangles (iNFTs). They were also not observed around late stage
eNFTs. The TANCs contained both type 1 (elongated) and type 2 (globular) dystrophic neurites, as well as small, granular structures.
The type 1 dystrophic neurites in TANCs were immunostained by antibodies to neuroskeletal proteins, while type 2 dystrophic
neurites were immunostained by antibodies to amyloid precursor protein (APP). The eNFTs surrounded by TANCs were almost all
immunopositive for amyloid P, while only some were immunopositive for C4d, and only a minority had β-amyloid protein (Aβ)
associated with them. We hypothesize that the eNFTs are a source of complement activation which results in destruction of
surrounding neurites. We further hypothesize that the degenerating neurites are a source of Aβ which forms long-term deposits
around eNFTs.
Received: 10 March 1997 / Accepted: 7 May 1997 |
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Keywords: | Degenerated neurites Ghost tangles Bodig disease Alzheimer’ s disease β -amyloid protein |
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