Regulating cholesterol levels in the brain decreases levels of the Amyloid-beta peptide, according to research published this week by the EMBO journal. This peptide is thought to be the causative agent involved in the pathology of Alzheimer's disease.
In the study, by Hasan Mohajeri and colleagues, experiments performed in the mouse brain show for the first time in vivo that interfering with the activity of an enzyme required for the cholesterol production, seladin-1, leads to an increase in Amyloid-beta formation. Conversely, the authors show that increasing seladin-1 levels in cultured human neuroblastoma cells reduces Amyloid-beta levels.
In the normal situation, special cholesterol-rich territories of the membrane physically separate the precursor of Amyloid-beta peptide from the enzymes that are necessary for the generation of the peptide. In the absence of selanin-1, cholesterol levels are low and these territories are disorganized, leaving the enzymes free to process the precursor of Amyloid-beta peptide and form more of the toxic product.
Recent studies have implicated cholesterol metabolism in the pathophysiology of Alzheimer?s disease. The mechanism by which cholesterol modulates the production of the toxic beta-amyloid peptide has however so far remained elusive.
This study nicely confirms that seladin-1 play a crucial role in Amyloid-beta peptide production in vivo, and indicates that pharmacological enhancement of seladin-1 activity may be a novel therapeutic strategy for Alzheimer’s disease.
Hasan Mohajeri (University of Zurich, Zurich, Switzerland)
Lola Ledesma, (Cavalieri Ottolenghi Scientific Institute, Turin, Italy)
Abstract available online.
(C) EMBO journal press release.
Message posted by: Trevor M. D'Souza
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