B. M. Austen*, C. Sidera, C. Liu, E. Frears

Correspondence: Neurodegeneration Unit, Dept of Surgery, St George's Hospital Medical School, Cranmer Terrace, LONDON SW17 ORE. Telephone 02087255651. Fax: 02087253594. Email sghk200@sghms.ac.uk

The objectives of this article are to summarise evidence that amyloidogenesis is a causal factor in Alzheimer's disease, to outline the main pathways of amyloidogenesis in Alzheimer's disease, describe contemporary evidence showing that the processing of the amyloid precursor protein and amyloidogenesis is strongly influenced by the levels of intracellular cholesterol. Moreover, we shall suggest a mechanistic hypothesis that could explain the observed epidemiological links between the use of inhibitors of cholesterol biosynthesis in patients and the observed reduced risk of Alzheimer's disease.

Key Words: Cholesterol, beta-amyloid, nutrition, aging, Alzheimer's disease, lovastatin, elderly.