Article

In search for individualized predictors of stroke recovery, the Val66Met
polymorphism of the brain-derived neurotrophic factor (BDNF) is attracting great
interest, because it has a negative impact on neurotrophin function. Since stroke
recovery relies on brain plastic processes, on which BDNF is permissive, the
dominant thought is in favor of a worse recovery in Met carriers. Conversely, we
suggest that Met carriers do not differ in terms of absolute ability to recover
from stroke, but they do differ on the way they recover. In particular, Met
carriers rely more on subcortical plasticity, while ValVal patients more on
intracortical plastic processes. Indeed, the direct evidence of impaired Met
carrier recovery is inconsistent, as a high worldwide diffusion of the
polymorphism suggests. The plasticity taking place in cortex, which is the one
targeted by noninvasive brain stimulation strategies aimed at enhancing recovery,
is less pronounced in Met carrier stroke patients, who have instead spared global
recovery potential. Enhanced subcortical plasticity sustains better stroke
recovery of Met carrier mice: this may also happen in humans, explaining the
weaker interhemispheric cortical excitability imbalance recently described in Met
carriers. Thus, BDNF haplotype determines mechanisms and structures involved in
stroke recovery. The less pronounced cortical plasticity of Met carrier implies
that plastic changes induced by interventional neurophysiological protocols would
be better predictors of ValVal chronic outcome and those protocols would be more
effective to boost their recovery. Other strategies, more focused on subcortical
mechanisms, should be used in Met carriers.
CI - (c) The Author(s) 2015.

Langue : ANGLAIS