Received 19 October 2009; received in revised form 8 December 2009; accepted 16 December 2009. published online 15 January 2010. Corrected Proof
Background
The brain-derived neurotrophic factor (BDNF) gene is involved in mechanisms of synaptic plasticity in the adult brain. It has been demonstrated that BDNF also plays a significant role in shaping externally induced human brain plasticity. Plasticity induced in the human motor cortex by intermittent theta-burst stimulation (iTBS) was impaired in individuals expressing the Val66Met polymorphism.
Methods
To explore whether this polymorphism is also important for other neuroplasticity-inducing tools in humans with modes of action differing from that of iTBS, namely, transcranial direct current (tDCS) and random noise stimulation (tRNS), we retrospectively analyzed the data of 64 subjects studied in our laboratory with regard to BDNF genotype.
Results
Fifteen subjects with the Val66Met allele, 46 subjects with the Val66Val allele, and 3 Met66Met carriers were identified. The response of the Val66Met allele carriers to stimulation differed in two protocols compared with the response of Val66Val individuals. For iTBS (15 subjects, 5 heterozygotes), plasticity could be only induced in the Val66Val allele carriers. However, for facilitatory tDCS (24 subjects, 10 heterozygotes), as well as for inhibitory tDCS, (19 subjects, 8 heterozygotes), carriers of the Val66Met allele displayed enhanced plasticity, whereas for transcranial random noise stimulation (29 subjects, 8 heterozygotes), the difference between groups was not so pronounced.
Conclusions
BDNF polymorphism has a definite impact on plasticity in humans, which might differ according to the mechanism of plasticity induction. This impact of BDNF on plasticity should be taken into account for future studies, as well as having wider ranging implications for the treatment of neuropsychiatric disorders with transcranial stimulation tools, as it may predetermine their efficacy for the treatment of disease and rehabilitation.
aDepartment of Clinical Neurophysiology, Georg-August University of Göttingen, Göttingen, Germany
bInstitute of Human Genetics, Georg-August University of Göttingen, Göttingen, Germany
Correspondence: Andrea Antal, PhD, Department of Clinical Neurophysiology, Georg-August University, Robert-Koch-Str. 40, 37075 Göttingen, Germany.
This study was initiated and funded by an unrestricted grant awarded by the Rose Foundation (L.C./W.P.) and by the Bernstein Center for Computational Neuroscience Göttingen (V.M./W.P.) (BMBF 01GQ0782).
ABSTRACT