alpha-synuclein inclusions in amygdala in the brains of patients with the Parkinsonism-dementia complex of Guam

Citation
M. Yamazaki et al., alpha-synuclein inclusions in amygdala in the brains of patients with the Parkinsonism-dementia complex of Guam, J NE EXP NE, 59(7), 2000, pp. 585-591
Citations number
36
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
ISSN journal
00223069 → ACNP
Volume
59
Issue
7
Year of publication
2000
Pages
585 - 591
Database
ISI
SICI code
0022-3069(200007)59:7<585:AIIAIT>2.0.ZU;2-C
Abstract
We investigated by immunohistochemistry the deposition of alpha-synuclein i n the brains of deceased patients with the parkinsonism-dementia complex (P DC) of Guam. Five of 13 PDC brains showed numerous alpha-synuclein positive neuronal inclusions and abnormal neurites, chiefly in the amygdala. Simila r alpha-synuclein positive lesions were observed, although to a lesser exte nt, in the entorhinal cortex and the dorsal vagal nucleus. No a-synuclein p ositive inclusions were observed in motor cortex or locus coeruleus, and on ly a small number of positive inclusions were found in the Sommer's sector, temporal cortex, or substantia nigra. Some of the alpha-synuclein positive inclusions were reminiscent of cortical Lewy bodies (LB), but many of thos e in the amygdala coexisted with tan-positive pretangles and/or neurofibril lary tangles (NFT) within the same neurons. In these neurons, tan-positive shells encapsulated alpha-synuclein positive central cores or irregularly s haped alpha-synuclein-positive deposition intermingled with pretangles/NFT. Thus, the present study suggests that a common mechanism may govern aggreg ation of alpha-synuclein and tau in the amygdala, and that aggregation of a lpha-synuclein may play some role in the neurodegenerative process of a tau opathy (i.e. PDC) in which A beta deposition is virtually absent.