Does TMS Affect Neuroplasticity? The Role of Brain-derived Neurotrophic Factor and Neuronal Cell Adhesion Molecules - an Intensive Clinical Protocol Among Patients With Obsessive-compulsive Disorders

Transcranial Magnetic Stimulation (TMS) is an accepted non-invasive method of neurostimulation. Evidence has demonstrated that TMS allows for the reduction of depression symptoms, and an increasing number of reports support its efficacy in reducing symptoms of obsessive-compulsive disorder (OCD). There is a limited body of clinical research available on the mechanisms of TMS action. Neuroplasticity refers to the capacity of neural tissue to form new connections for the purpose of reorganization and adaptation. Brain-Derived Neurotrophic Factor (BDNF) and Cell Adhesion Molecules (CAM) are markers of neuroplasticity. BDNF influences transmission in both excitatory and inhibitory synapses, enhancing neurotransmitter release in cholinergic and dopaminergic neurons. According to the neurotrophic hypothesis, stress may decrease BDNF levels. Serum BDNF concentrations are reduced in untreated patients with depression and normalized by antidepressant treatment. Neuronal CAMs are among the most prevalent proteins, playing a crucial role in synaptic plasticity. Various CAMs appear to interact with BDNF. In depression, both reduced BDNF levels and polysialylated (PSA) neuronal CAMs are observed. Conversely, the levels of Vascular Cell Adhesion Molecule-1 (VCAM-1) and Intracellular Adhesion Molecule-1 (ICAM-1) in depression are inversely correlated with BDNF.

To address this gap, the investiagators aimed to verify the hypothesis that TMS in OCD leads to symptom reduction by inducing neuroplasticity through:

Comparing changes in BDNF and CAM protein concentrations after TMS stimulation in OCD patients before and after stimulation.

Assessing the correlation between changes in BDNF and CAM concentrations and the reduction of psychopathological symptoms.

Evaluating the predictive value of initial BDNF and CAM concentrations.