Premium
A pathological study of Lewy bodies and senile changes in the amygdala in diffuse Lewy body disease
Author(s) -
Iseki Eizo,
Odawara Toshinari,
Suzuki Kyoko,
Kosaka Kenji,
Akiyama Haruhiko,
Ikeda Kenji
Publication year - 1995
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.1995.tb00252.x
Subject(s) - pathology , senile plaques , lewy body , locus ceruleus , amygdala , substantia nigra , atrophy , alzheimer's disease , medicine , dementia , parkinson's disease , disease
A quantitative study of the distribution and incidence of Lewy bodies (LB) and senile changes was performed in seven subnuclei of the amygdala in 12 cases with diffuse Lewy body disease (DLBD). The results were compared with those in six cases of idiopathic Parkinson's disease (PD), six cases of Alzheimer‐type dementia (ATD) and six cases of non‐demented controls. Ubiquitin immunohisto‐chemistry for LB, methenamine‐silver stain for senile plaques (SP) and Gallyas stain for neurofibrillary tangles (NFT) were used in this study. In all DLBD cases and four PD cases, cortical LB occurred in all subnuclei with a tendency for their preferential occurrence in certain sub‐nuclei. The probable dysfunction in these subnuclei may contribute to the memory impairment of DLBD. Senile plaques and NFT occurred significantly more frequently in the baso‐lateral nuclear group than in the cortico‐medial nuclear group of the amygdala in DLBD cases as well as in ATD cases, although a tendency for these to occur predominantly in certain subnuclei was not observed. In the central amygdaloid nucleus (CE), many characteristic spherical or fusiform structures were stained positively with ubiquitin immunohistochemistry in all DLBD and PD cases, although the number was less in PD cases. These immunohistochemically ubiquitin positive structures were densely packed electronmicroscopically with ubiquitin‐positive granular and vesicular components. They might have arisen from selective degeneration of the terminal or distal axons of noradrenergic and dopaminergic afferents from the locus ceruleus and substantia nigra, respectively, to the CE.