Background. Brain-derived neurotrophic factor (BDNF) is assumed to play a role in mediating neuroplasticity after stroke. Carriers of the function-limiting Val66Met (rs6265) single nucleotide polymorphism (SNP) may have a downregulation in BDNF secretion, which may lead to a poorer prognosis after stroke compared to noncarriers in motor learning and motor function recovery. The present study investigates whether this polymorphism may also affect the recovery of poststroke aphasia (ie, language impairment). Objective. To study the influence of the BDNF Val66Met polymorphism on the recovery of poststroke aphasia. Methods. We included 53 patients with poststroke aphasia, all participating in an inpatient rehabilitation program with speech and language therapy. All patients were genotyped for the Val66Met SNP and subdivided into carriers (at least one Met al.lele) and noncarriers (no Met al.lele). Primary outcome measures included the improvement over rehabilitation time on the Amsterdam-Nijmegen Everyday Language Test (ANELT) and the Boston Naming Test (BNT). Results. The outcome measures showed a large variability in the improvement scores on both the ANELT and BNT. There was no significant difference between noncarriers and carriers in the primary outcome measures. Conclusion. This study investigated the effect of the BDNF Val66Met polymorphism on clinical recovery of poststroke aphasia. In contrast to earlier studies describing a reducing effect of this polymorphism on motor function recovery after stroke, the present study does not support a reduction in language recovery for carriers compared to noncarriers with poststroke aphasia.

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Keywords aphasia, brain-derived neurotrophic factor, neuroplasticity, single nucleotide polymorphism, stroke
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Journal Neurorehabilitation and Neural Repair
De Boer, R.G.A. (Riemke), Spielmann, K, Heijenbrok-Kal, M.H, Van Der Vliet, R, Ribbers, G.M, & van de Sandt-Koenderman, W.M.E. (2017). The Role of the BDNF Val66Met Polymorphism in Recovery of Aphasia after Stroke. Neurorehabilitation and Neural Repair, 31(9), 851–857. doi:10.1177/1545968317723752