期刊
ACTA NEUROPATHOLOGICA
卷 119, 期 5, 页码 567-577出版社
SPRINGER
DOI: 10.1007/s00401-010-0657-2
关键词
Dystrophic neurites; Demyelination; A beta plaques; Degeneration; Alzheimer's disease
资金
- Australian National Health and Medical Research Council
- J.O. and J.R. Wicking Trust (ANZ Charitable Services)
We have investigated alterations in myelin associated with A beta plaques, a major pathological hallmark of Alzheimer's disease (AD), in human tissue and relevant transgenic mice models. Using quantitative morphological techniques, we determined that fibrillar A beta pathology in the grey matter of the neocortex was associated with focal demyelination in human presenilin-1 familial, sporadic and preclinical AD cases, as well as in two mouse transgenic models of AD, compared with age-matched control tissue. This demyelination was most pronounced at the core of A beta plaques. Furthermore, we found a focal loss of oligodendrocytes in sporadic and preclinical AD cases associated with A beta plaque cores. In human and transgenic mice alike, plaque-free neocortical regions showed no significant demyelination or oligodendrocyte loss compared with controls. Dystrophic neurites associated with the plaques were also demyelinated. We suggest that such plaque-associated focal demyelination of the cortical grey matter might impair cortical processing, and may also be associated with aberrant axonal sprouting that underlies dystrophic neurite formation.
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