Topic: intermittent theta burst stimulation

Transcranial magnetic stimulation (TMS) is a non-invasive brain stimulation technique for modulating neocortical excitability in humans. Repetitive magnetic stimulations (rMS) applied to tissue cultures trigger functional changes of dendritic spines alongside a potentiation of excitatory neurotransmission. Furthermore, in vivo studies involving both animal models and patients have demonstrated the therapeutic potential of rTMS in treating psychiatric disorders.Despite its use in both neuroscience research and clinical settings, the molecular mechanisms of rTMS-based interventions remain not we

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and caudoputamen (Cp), leading to motor and non-motor symptoms. Neuroinflammation, oxidative stress, and imbalance in purinergic signaling significantly contribute to its progression. Current treatments fail to halt disease progression, necessitating novel approaches. Repetitive transcranial magnetic stimulation (rTMS) has shown promise in alleviating PD symptoms, but its underlying mechanisms remain unclear. We investigated the effects of prolonged intermitten

Intermittent theta burst stimulation (iTBS), a specialized protocol of repetitive transcranial magnetic stimulation (rTMS), is a non-invasive method used to study brain function in health and disease in both animal models and humans. Despite increasing interest, fundamental questions regarding the cellular and molecular effects of iTBS/rTMS on brain activity remain unanswered. It is generally recognized that c-Fos can be used as a molecular marker of neuronal activity following different types of stimuli. Therefore, this study aimed to investigate the effects of seven-day iTBS application on c

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to reduced striatal dopamine and motor and non-motor symptoms. The imbalance of adenosine signaling plays a role in the pathogenesis of PD, particularly through increased A2AR and reduced A1R activity affecting D2R and D1R signaling pathways, respectively. This imbalance interferes with the reciprocal modulation of adenylate cyclase by A1R/D1R and A2AR/D2R and impairs motor control. Despite existing treatment options, there is an unmet need for new interve