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Brain fatty acid uptake is a critical physiological process rather than a single molecular target. It describes the mechanism by which essential long-chain fatty acids (LCFAs), such as docosahexaenoic acid (DHA) and arachidonic acid, cross the blood-brain barrier (BBB) to support neural function [PubMed: 25231861]. The brain is unable to synthesize these essential fats de novo and relies on uptake mediated by specialized proteins, most notably Major Facilitator Superfamily Domain Containing 2A (MFSD2A), which specifically transports DHA in the form of lysophosphatidylcholine [Nature, 2014]. Other contributors to this process include Fatty Acid Transport Proteins (FATPs), CD36, and Fatty Acid Binding Proteins (FABPs) [NIH: PMC4245570]. Dysregulation of this uptake process is heavily implicated in neurodegenerative diseases like Alzheimer's and structural brain defects such as microcephaly [UniProt: Q8NA29]. Pharmacological efforts in this area focus on enhancing the delivery of omega-3 fatty acids or modulating transporter activity to treat cognitive decline and neurodevelopmental disorders.
Facilitated transport of long-chain fatty acids across the blood-brain barrier via specific membrane transporters such as MFSD2A and CD36.
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