Co-localization of cholesterol, apolipoprotein E and fibrillar Abeta in amyloid plaques.
Recent evidence strongly suggests a role for cholesterol and apolipoprotein E in the etiology of Alzheimer's disease. We have demonstrated the co-localization of cholesterol and apolipoprotein E with beta-amyloid immunoreactivity and thioflavin S immunofluorescence in AD type plaques of a transgenic mouse model. Cholesterol and apolipoprotein E co-localized to the core of thioflavin S-positive (fibrillar) plaques, but not thioflavin S-negative (diffuse) plaques from an early age. By 18 months of age, there was extensive coverage of fibrillar plaques immunopositive for apolipoprotein E and cholesterol oxidase. These findings support evidence that cholesterol and apolipoprotein E are involved in fibrillar plaque formation or maintenance, and suggest that cholesterol may impact amyloid formation extracellularly, as well as through an intracellular effect.
Burns
Mark P
MP
Center for Dementia Research, Nathan S. Kline Institute, 140 Old Orangeburg Rd, Orangeburg, NY 10962, USA. burns@nki.rfmh.org
Noble
Wendy J
WJ
Olm
Vicki
V
Gaynor
Kate
K
Casey
Evelyn
E
LaFrancois
John
J
Wang
Lili
L
Duff
Karen
K
D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000032:analysis*; D000818:Animals; D001057:Apolipoproteins E / Q000032:analysis*; D002784:Cholesterol / Q000032:analysis*; D007150:Immunohistochemistry; D051379:Mice; D008817:Mice, Mutant Strains; D058225:Plaque, Amyloid / Q000737:chemistry* / Q000473:pathology
D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D002784:Cholesterol