Mitochondria, cholesterol and amyloid β peptide: a dangerous trio in Alzheimer disease View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2009-09-26

AUTHORS

Anna Colell, Anna Fernández, José C. Fernández-Checa

ABSTRACT

The molecular mechanisms of Alzheimer’s disease (AD) are not fully understood. Extensive evidence from experimental models has involved the overgeneration and accumulation of toxic amyloid β peptides (Aβ) in the onset and progression of the disease. The amyloidogenic processing of amyloid precursor protein into pathogenic Aβ fragments is thought to occur in specific domains of the plasma membrane and favored by cholesterol enrichment. Intracellular Aβ accumulation is known to induce oxidative stress, predominantly via mitochondria targeting of toxic Aβ. Recent evidence using mouse models of cholesterol loading has demonstrated that the specific mitochondrial cholesterol pool sensitizes neurons to Aβ-induced oxidant cell death and caspase-independent apoptosis due to selective mitochondrial GSH (mGSH) depletion induced by cholesterol-mediated perturbation of mitochondrial membrane dynamics. mGSH replenishment by permeable precursors such as glutathione ethyl ester protected against Aβ-mediated neurotoxicity and inflammation. Thus, these novel data expand the pathogenic role of cholesterol in AD indicating that in addition to fostering Aβ generation, mitochondrial cholesterol determines Aβ neurotoxicity via mGSH regulation. More... »

PAGES

417

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10863-009-9242-6

DOI

http://dx.doi.org/10.1007/s10863-009-9242-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005321582

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19784764


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