Alpha-linolenic acid given as enteral or parenteral nutritional intervention against sensorimotor and cognitive deficits in a mouse model of ischemic stroke.

Key Findings

Stroke survivors have a high level of disability with more than 50% of patients being left with a residual motor or cognitive/amnesic deficit. ALA supplementation either as an i.v. treatment or as enriched-diet enhances brain plasticity and improves neurite growth and remodeling in hippocampal neurons (a main site for memory formation). In this study, the effects of ALA on post-stroke rehabilitation, that is recovery of motor and cognitive functions after stroke, were assessed in the 30 min MCAo model. Dietary ALA supplementation improved short-term post-stroke body weight and motor recovery. ALA-diet fed mice and ALA-injected mice took significantly less time and exhibited optimized searching behaviors compared with the mice fed the regular diet or treated with the vehicle. These findings suggest that ALA improves the spontaneous recovery of spatial learning and memory in a mouse model of ischemic stroke. Controlled studies are suggested to confirm the value of ALA in post stroke ailments.

ABSTRACT

Stroke is a leading cause of disability and death worldwide. Numerous therapeutics applied acutely after stroke have failed to improve long-term clinical outcomes. An emerging direction is nutritional intervention with omega-3 polyunsaturated fatty acids acting as disease-modifying factors and targeting post-stroke disabilities. Our previous studies demonstrated that the omega-3 precursor, alpha-linolenic acid (ALA) administrated by injections or dietary supplementation reduces stroke damage by direct neuroprotection, and triggering brain artery vasodilatation and neuroplasticity. Successful translation of putative therapies will depend on demonstration of robust efficacy on common deficits resulting from stroke like loss of motor control and memory/learning. This study evaluated the value of ALA as adjunctive therapy for stroke recovery by comparing whether oral or intravenous supplementation of ALA best support recovery from ischemia. Motor and cognitive deficits were assessed using rotarod, pole and Morris water maze tests. ALA supplementation in diet was better than intravenous treatment in improving motor coordination, but this improvement was not due to a neuroprotective effect since infarct size was not reduced. Both types of ALA supplementation improved spatial learning and memory after stroke. This cognitive improvement correlated with higher survival of hippocampal neurons. These results support clinical investigation establishing therapeutic plans using ALA supplementation. Stroke survivors have a high level of disability with more than 50% of patients being left with a residual motor or cognitive/amnesic deficit.