Journal
BRAIN RESEARCH BULLETIN
Volume 53, Issue 4, Pages 389-397Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0361-9230(00)00370-1
Keywords
prion disease; cholesterol; amylin; membrane lipid; conformational disease
Categories
Ask authors/readers for more resources
The etiology of Alzheimer's disease has been suggested to be linked to the neurodegeneration induced by B-amyloid protein (A betaP), however, the mechanism underlying the latter remains unknown. We have previously shown the direct incorporation of A betaP into neuronal membranes of immortalized hypothalamic neurons (GT1-7 cells) associated with the formation of calcium-permeable pores, and the elevation of the intracellular calcium concentrations in the GT1-7 cells. Taking together our results and those of numerous other studies, we hypothesize that the disruption of calcium homeostasis by A betaP-channels may be the molecular basis of the neurotoxicity of A betaP, and the development of Alzheimer's disease. it is also proposed that the constituents of membrane lipids may play important roles in the process of this channel formation. Our hypothesis may also explain the mechanism of development of other 'conformational diseases', such as prion disease or type 2 diabetes mellitus, which share some common features with Alzheimer's disease. (C) 2000 Elsevier Science Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available