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JSLHR-L-RSNP-19-0021Kristinsson_SuppS1.pdf (57.37 kB)

BDNF genotype & brain activation in aphasia (Kristinsson et al., 2019)

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posted on 2019-11-22, 20:32 authored by Sigfus Kristinsson, Grigori Yourganov, Feifei Xiao, Leonardo Bonilha, Brielle C. Stark, Chris Rorden, Alexandra Basilakos, Julius Fridriksson
Purpose: The brain-derived neurotrophic factor (BDNF) gene has been shown to be important for synaptic plasticity in animal models. Human research has suggested that BDNF genotype may influence stroke recovery. Some studies have suggested a genotype-specific motor-related brain activation in stroke recovery. However, recovery from aphasia in relation to BDNF genotype and language-related brain activation has received limited attention. We aimed to explore functional brain activation by BDNF genotype in individuals with chronic aphasia. Consistent with findings in healthy individuals and individuals with poststroke motor impairment, we hypothesized that, among individuals with aphasia, the presence of the Met allele of the BDNF gene is associated with reduced functional brain activation compared to noncarriers of the Met allele.
Method: Eighty-seven individuals with chronic stroke-induced aphasia performed a naming task during functional magnetic resonance imaging scanning and submitted blood or saliva samples for BDNF genotyping. The mean number of activated voxels was compared between groups, and group-based activation maps were directly compared. Neuropsychological testing was conducted to compare language impairment between BDNF genotype groups. The Western Aphasia Battery Aphasia Quotient (Kertesz, 2007) was included as a covariate in all analyses.
Results: While lesion size was comparable between groups, the amount of activation, quantified as the number of activated voxels, was significantly greater in noncarriers of the Met allele (whole brain: 98,500 vs. 28,630, p < .001; left hemisphere only: 37,209 vs. 7,000, p < .001; right hemisphere only: 74,830 vs. 30,630, p < .001). This difference was most strongly expressed in the right hemisphere posterior temporal area, pre- and postcentral gyrus, and frontal lobe, extending into the white matter. Correspondingly, the atypical BDNF genotype group was found to have significantly less severe aphasia (Western Aphasia Battery Aphasia Quotient of 64.2 vs. 54.3, p = .033) and performed better on a naming task (Philadelphia Naming Test [Roach, Schwartz, Martin, Grewal, & Brecher, 1996] score of 74.7 vs. 52.8, p = .047). A region of interest analysis of intensity of activation revealed no group differences, and a direct comparison of average activation maps across groups similarly yielded null results.
Conclusion: BDNF genotype mediates cortical brain activation in individuals with chronic aphasia. Correspondingly, individuals carrying the Met allele present with more severe aphasia compared to noncarriers. These findings warrant further study into the effects of BDNF genotype in aphasia.

Supplemental Material S1. Apraxia measures for a subsample of 65 participants from Fridriksson et al. (2018).

Kristinsson, S., Yourganov, G., Xiao, F., Bonilha, L., Stark, B. C., Rorden, C., ... Fridriksson, J. (2019). Brain-derived neurotrophic factor genotype–specific differences in cortical activation in chronic aphasia. Journal of Speech, Language, and Hearing Research, 62, 3923-3936.

Publisher Note: This article is part of the Forum: Advances in Neuroplasticity Research on Language Recovery in Aphasia.


This article stems from the 2018 Research Symposium at the American Speech-Language-Hearing Association Convention, which was supported by the National Institute on Deafness and Other Communication Disorders of the National Institutes of Health under Award R13DC003383. The study was supported by the National Institute on Deafness and Other Communication Disorders Award P50 DC014664 and U01 DC011739 (PI: Fridriksson).