|
| Authors, year | Study design, sample size, mean age | Stroke type | BDNF genotypes | Intervention | Outcome assessment | Results/findings |
|
| de Boer et al., 2017 [10] | Prospective cohort study, 53 subjects, 58.5 years | Acute (ischemic and hemorrhagic) | (i) Val66Met allele present
(ii) Val66Met allele absent | SLT for 2-5 hours per week | (1) ANELT
(2) BNT | No significant differences between carriers of both alleles in improvement scores on both the ANELT and BNT |
| Fridriksson et al., 2018 [11] | Randomized controlled trial, 74 subjects (BDNF genotype available for 67), 61.7 years | Acute (ischemic and hemorrhagic) | (i) Atypical (Val/Met, Met/Met)
(ii) Typical (Val/Val) | Received either 1 mA A-tDCS or sham tDCS for 20 mins per session for 5×/week for 3 weeks | (1) Naming 80
(2) PNT
(3) WAB-R AQ | Atypical BDNF carriers showed significantly poorer response to A-tDCS than typical BDNF carriers who received both A-tDCS and S-tDCS
Atypical BDNF carriers associated with poorer AQ scores at baseline compared to typical BDNF carriers |
| Kristinsson et al., 2019 [12] | Cross-sectional study, 87 subjects, 61.7 years | Chronic (ischemic and hemorrhagic) | (i) Atypical (Val66Met, Met66Met)
(ii) Typical (Val66Val) | Not applicable | (1) WAB AQ
(2) PNT
(3) fMRI activation map analysis
(4) Activated voxels at the whole-brain level | Atypical BDNF carriers significantly have more severe aphasia on WAB-AQ and performed significantly better in PNT compared to typical BDNF carriers
No group differences between intensity of cortical activation across both groups
The number of activated voxels was significantly lower in atypical BDNF carriers compared to typical BDNF carriers |
|
