Enhancing docosahexaenoic acid transport across the blood-brain barrier to improve cognitive function in Alzheimer's disease

Alzheimer's disease (AD), the leading cause of dementia with no current cure, is associated with lower brain levels of the cognitively-beneficial fatty acid docosahexaenoic acid (DHA). As the brain has a limited capacity to produce its own DHA, the majority of brain DHA is derived from the plasma, and so DHA trafficking across the blood-brain barrier (BBB) is essential to maintain brain levels of DHA, and therefore, cognitive function. We have previously demonstrated that the BBB transport of DHA is significantly reduced in a mouse model of familial AD and have associated this with reduced levels of transporters essential for this process. Our laboratory is currently investigating approaches to restore the expression and function of these carrier proteins, which is expected to result in increased brain access of DHA and improved cognitive function in AD, ultimately of benefit for the significant number of individuals with this disease.

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