OBJECTIVES: The ability of noninvasive brain stimulation to modulate corticospinal excitability and plasticity is influenced by genetic predilections such as the coding for brain-derived neurotrophic factor (BDNF). Otherwise healthy individuals presenting with BDNF Val66Met (Val/Met) polymorphism are less susceptible to changes in excitability in response to repetitive transcranial magnetic stimulation (TMS) and paired associative stimulation paradigms, reflecting reduced neuroplasticity, compared to Val homozygotes (Val/Val). In the current study, we investigated whether BDNF polymorphism influences "baseline" excitability under TMS conditions that are not repetitive or plasticity-inducing. Cross-sectional BDNF levels could predict TMS response more generally because of the ongoing plasticity processes. MATERIALS AND METHODS: Forty-five healthy individuals (23 females; age: 25.3 ± 7.0 years) participated in the study, comprising two groups. Motor evoked potentials (MEP) were collected using single-pulse TMS paradigms at fixed stimulation intensities at 110% of the resting motor threshold in one group, and individually-derived intensities based on MEP sizes of 1 mV in the second group. Functional variant Val66Met (rs6265) was genotyped from saliva samples by a technician blinded to the identity of DNA samples. RESULTS: Twenty-seven participants (60.0%) were identified with Val/Val, sixteen (35.5%) with Val/Met genotype, and two with Met/Met genotype. MEP amplitudes were significantly diminished in the Val/Met than Val/Val individuals. These results held independent of the single-pulse TMS paradigm of choice (p = 0.017110% group; p = 0.035 1 mV group), age, and scalp-to-coil distances. CONCLUSIONS: The findings should be further substantiated in larger-scale studies. If validated, intrinsic differences by BDNF polymorphism status could index response to TMS prior to implementing plasticity-inducing protocols.
OBJECTIVES: The ability of noninvasive brain stimulation to modulate corticospinal excitability and plasticity is influenced by genetic predilections such as the coding for brain-derived neurotrophic factor (BDNF). Otherwise healthy individuals presenting with BDNF Val66Met (Val/Met) polymorphism are less susceptible to changes in excitability in response to repetitive transcranial magnetic stimulation (TMS) and paired associative stimulation paradigms, reflecting reduced neuroplasticity, compared to Val homozygotes (Val/Val). In the current study, we investigated whether BDNF polymorphism influences "baseline" excitability under TMS conditions that are not repetitive or plasticity-inducing. Cross-sectional BDNF levels could predict TMS response more generally because of the ongoing plasticity processes. MATERIALS AND METHODS: Forty-five healthy individuals (23 females; age: 25.3 ± 7.0 years) participated in the study, comprising two groups. Motor evoked potentials (MEP) were collected using single-pulse TMS paradigms at fixed stimulation intensities at 110% of the resting motor threshold in one group, and individually-derived intensities based on MEP sizes of 1 mV in the second group. Functional variant Val66Met (rs6265) was genotyped from saliva samples by a technician blinded to the identity of DNA samples. RESULTS: Twenty-seven participants (60.0%) were identified with Val/Val, sixteen (35.5%) with Val/Met genotype, and two with Met/Met genotype. MEP amplitudes were significantly diminished in the Val/Met than Val/Val individuals. These results held independent of the single-pulse TMS paradigm of choice (p = 0.017110% group; p = 0.035 1 mV group), age, and scalp-to-coil distances. CONCLUSIONS: The findings should be further substantiated in larger-scale studies. If validated, intrinsic differences by BDNF polymorphism status could index response to TMS prior to implementing plasticity-inducing protocols.
Authors: K A McConnell; Z Nahas; A Shastri; J P Lorberbaum; F A Kozel; D E Bohning; M S George Journal: Biol Psychiatry Date: 2001-03-01 Impact factor: 13.382
Authors: P M Rossini; A T Barker; A Berardelli; M D Caramia; G Caruso; R Q Cracco; M R Dimitrijević; M Hallett; Y Katayama; C H Lücking Journal: Electroencephalogr Clin Neurophysiol Date: 1994-08
Authors: P Li Voti; A Conte; A Suppa; E Iezzi; M Bologna; M S Aniello; G Defazio; J C Rothwell; Alfredo Berardelli Journal: Exp Brain Res Date: 2011-05-03 Impact factor: 1.972
Authors: Jeffrey A Kleim; Sheila Chan; Erin Pringle; Kellan Schallert; Vincent Procaccio; Richard Jimenez; Steven C Cramer Journal: Nat Neurosci Date: 2006-05-07 Impact factor: 24.884
Authors: Lukas Pezawas; Beth A Verchinski; Venkata S Mattay; Joseph H Callicott; Bhaskar S Kolachana; Richard E Straub; Michael F Egan; Andreas Meyer-Lindenberg; Daniel R Weinberger Journal: J Neurosci Date: 2004-11-10 Impact factor: 6.167
Authors: F Miyajima; W Ollier; A Mayes; A Jackson; N Thacker; P Rabbitt; N Pendleton; M Horan; A Payton Journal: Genes Brain Behav Date: 2007-10-31 Impact factor: 3.449
Authors: Stephanie A McHughen; Paul F Rodriguez; Jeffrey A Kleim; Erin D Kleim; Laura Marchal Crespo; Vincent Procaccio; Steven C Cramer Journal: Cereb Cortex Date: 2009-09-10 Impact factor: 5.357
Authors: Haley C Dresang; Denise Y Harvey; Sharon X Xie; Priyanka P Shah-Basak; Laura DeLoretta; Rachel Wurzman; Shreya Y Parchure; Daniela Sacchetti; Olufunsho Faseyitan; Falk W Lohoff; Roy H Hamilton Journal: Neurorehabil Neural Repair Date: 2022-04-15 Impact factor: 4.895