In recent years, the expression and modulation of neurotropic genes, both normal and mutated, have been postulated as potential prognostic markers. The brain-derived neurotrophic factor (BDNF) protein is a member of the nerve growth factor family of neurotrophins and is known to be essential for the development and maintenance of the neurons.
Missense mutations within this gene are also known to influence both axonal and dendritic morphology where the ocular dominance column development and initial dendritic outgrowth are altered. In search for individualized predictors of recovery, genetic factors are recently attracting great interest, in particular, the ones related to the brain-derived neurotrophic factor (BDNF).
To date, whether subjects heterozygote or homozygote for the Val66Met substitution (from now on Met carriers) have a worse outcome after stroke is matter of debate. After stroke, brain BDNF levels increase, affecting neuronal survival, differentiation, and use-dependent plasticity.
Of particular interest is the effect of rTMS on the regulation of brain-derived neurotrophic factor (BDNF), a potent trophic factor implicated in synaptic plasticity, neuronal survival, and regeneration. The role of BDNF in TMS-induced plasticity has gained significant attention in the clinical context because humans with genetic variants of BDNF respond differently to TMS protocols, providing a potential biomarker for tailoring treatment. Although the mechanism underpinning the different response in BDNF variants remains unknown, it seems that BDNF plays a key role in the effects of rTMS.

GENETIC ASPECTS OF TRANSCRANIAL MAGNETIC STIMULATION INDUCED BRAIN NEUROPLASTICITY IN ISCHEMIC STROKE PATIENTS