Abstract
Brain-Derived Neurotrophic Factor (BDNF) and its rs6265 single nucleotide polymorphism (SNP) play an important role in post-stroke recovery. We investigated the correlation between BDNF rs6265 SNP and recovery outcome, measured by the modified Barthel index, in 49 patients with stroke hospitalized in our rehabilitation center at baseline (T0) and after 30 sessions of rehabilitation treatment (T1); moreover, we analyzed the methylation level of the CpG site created or abolished into BDNF rs6265 SNP. In total, 11 patients (22.4%) were heterozygous GA, and 32 (65.3%) and 6 (12.2%) patients were homozygous GG and AA, respectively. The univariate analysis showed a significant relationship between the BDNF rs6265 SNP and the modified Barthel index cut-off (χ2(1, N = 48) = 3.86, p = 0.049), considering patients divided for carrying (A+) or not carrying (A−) the A allele. A higher percentage of A− patients obtained a favorable outcome, as showed by the logistic regression model corrected by age and time since the stroke onset, compared with the A+ patients (OR: 5.59). At baseline (T0), the percentage of BDNF methylation was significantly different between GG (44.6 ± 1.1%), GA (39.5 ± 2.8%) and AA (28.5 ± 1.7%) alleles (p < 0.001). After rehabilitation (T1), only patients A− showed a significant increase in methylation percentages (mean change = 1.3, CI: 0.4–2.2, p = 0.007). This preliminary study deserves more investigation to confirm if BDNF rs6265 SNP and its methylation could be used as a biological marker of recovery in patients with stroke undergoing rehabilitation treatment.
Highlights
Stroke is the primary cause of disability [1] and the second largest cause of death worldwide, with a high burden on patients, their families, and health-care systems [2]
We investigated whether Brain-Derived Neurotrophic Factor (BDNF) rs6265 polymorphism and the methylation status of the CpG site into this single nucleotide polymorphism (SNP) are involved in post-stroke recovery after rehabilitation treatment
48 patients were evaluated after the rehabilitation treatment
Summary
Stroke is the primary cause of disability [1] and the second largest cause of death worldwide, with a high burden on patients, their families, and health-care systems [2]. The brain has the ability to reorganize its neural networks, through neuroplasticity processes that include both the break-down and rewiring of the existing links, and the creation of new links [2] In this process, the Brain-Derived Neurotrophic Factor (BDNF), neurotrophin, which shows a very high expression in the brain [18,19,20], seems to have an important role, mainly in neuronal differentiation, survival, and synaptic plasticity. BDNF rs6265 is a single nucleotide polymorphism (SNP) G196A that produce a valine (Val) to methionine (Met) substitution at codon 66 (Val66Met) [28] This SNP modulates intracellular trafficking and BDNF secretion, associated with a reduced capacity for use-dependent plasticity in the motor cortex and impaired motor learning [29,30,31]. We investigated whether BDNF rs6265 polymorphism and the methylation status of the CpG site into this SNP are involved in post-stroke recovery after rehabilitation treatment
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