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We have investigated alterations in myelin associated with Ab 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 Ab 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 Ab plaques. Furthermore, we found a focal loss of oligodendrocytes in sporadic and preclinical AD cases associated with Ab 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.

Item Type:	Refereed Article
Keywords:	Dystrophic neurites; Demyelination; Abeta plaques; Degeneration; Alzheimer’s disease
Research Division:	Biomedical and Clinical Sciences
Research Group:	Neurosciences
Research Field:	Neurosciences not elsewhere classified
Objective Division:	Health
Objective Group:	Clinical health
Objective Field:	Clinical health not elsewhere classified
UTAS Author:	Mitew, S (Mr Stanislaw Mitew)
UTAS Author:	Kirkcaldie, MTK (Dr Matthew Kirkcaldie)
UTAS Author:	Vickers, JC (Professor James Vickers)
UTAS Author:	Dickson, TC (Professor Tracey Dickson)
ID Code:	64012
Year Published:	2010
Web of Science® Times Cited:	93
Deposited By:	Menzies Institute for Medical Research
Deposited On:	2010-06-16
Last Modified:	2013-07-16
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