FEBS Letters
Volume 580, Issue 23 , Pages 5525-5532, 9 October 2006

Amyloid excess in Alzheimer’s disease: What is cholesterol to be blamed for?

Edited by Bernard Helms

Department of Molecular and Developmental Genetics, Flanders Interuniversity Institute of Biotechnology (VIB11) and Catholic University of Leuven, Campus Gasthuisberg, Heerstraat 49, 3000 Leuven, Belgium

Received 8 June 2006; received in revised form 13 June 2006; accepted 14 June 2006. published online 23 June 2006.

Abstract 

A link between alterations in cholesterol homeostasis and Alzheimer’s disease (AD) is nowadays widely accepted. However, the molecular mechanism/s underlying such link remain unclear. Numerous experimental evidences support the view that changes in neuronal membrane cholesterol levels and/or subcellular distribution determine the aberrant accumulation of the amyloid peptide in the disease. Still, this view comes from rather contradictory data supporting the existence of either high or low brain cholesterol content. This is of particular concern considering that therapeutical strategies aimed to reduce cholesterol levels are already being tested in humans. Here, we review the molecular mechanisms proposed and discuss the perspectives they open.

Keywords: Cholesterol, Alzheimer’s disease, Membrane rafts, Amyloid peptide

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PII: S0014-5793(06)00745-9

doi:10.1016/j.febslet.2006.06.038

FEBS Letters
Volume 580, Issue 23 , Pages 5525-5532, 9 October 2006

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