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Cholesterol, statins and tau
Author(s) -
Ohm T. G.,
Meske V.
Publication year - 2006
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2006.00692.x
Subject(s) - cholesterol , neurodegeneration , alzheimer's disease , endocrinology , medicine , mevalonate pathway , metabolism , lipid metabolism , cholesterol synthesis , chemistry , disease , biochemistry , biosynthesis , reductase , enzyme
Many of the known risk factors for Alzheimer's disease (AD) are associated with cholesterol metabolism. Interestingly, it seems as if higher doses of statins, i.e. inhibitors of the cholesterol biosynthesis by blocking formation of mevalonate, might lower the progression of AD. The mechanisms, however, by which statins or cholesterol levels exert their influence are unknown. A hereditary cholesterol‐storage disorder, Niemann Pick C, shows Alzheimer‐like tau‐pathology in youth or adolescence but with no amyloid plaques. This gives rise to the possibility that disturbances in cholesterol metabolism induce changes in tau without interposition of A β ‐protein aggregates. Experimental data suggest that manipulation of cholesterol levels may lead to changes in tau phosphorylation. These changes vary depending on how cholesterol metabolism is manipulated. Effects seem to be either mild and transient, or drastic and related to neurodegeneration, or independent of the mevalonate pathway.