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
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.