A number of studies suggest a protective action of the fatty acid DHA in cognitive decline and in Alzheimer disease (AD). However, the molecular mechanism is not understood. In a paper appearing online on September 8 in advance of print publication of the October 1 issue of the Journal of Clinical Investigation, Nicolas Bazan and colleagues from Louisiana State University identify a specific mechanism by which DHA is neuroprotective in AD.
The authors report that DHA can decrease levels of the pathogenic Abeta peptides that are associated with Alzheimer disease pathology in human brain cells. Meanwhile, the synthesis of neuroprotectin D1 (NPD1), an endogenous DHA-derived messenger, is upregulated. NPD1 inhibits apoptosis triggered by Abeta peptides. In a human AD donor brain, the authors show that DHA and NPD1 are reduced in vulnerable brain regions.
This data raises the possibility that NPD1 is a key regulator of cell survival, and might be manipulated for the development of novel therapeutic strategies for neurodegenerative diseases.
TITLE: A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease
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