Bewegungstraining bei unipolarer Depression

41 Depressionspatienten nahmen an einem Bewegungsprogramm (physical activity, PA; N=23) oder einer Kontrollinvention (control intervention, CI; N=18) über jeweils 3 Wochen teil. Vor (Messung 1; M1) und nach (Messung 2; M2) diesem Interventionszeitraum wurden die Depressivität (Fragebögen: BDI-II / HAMD-17), Kognition (PC-gestützte Testbatterie) sowie kortikale Exzitabilität und LTP-ähnliche Plastizität (Transkranielle Magnetstimulation) gemessen. Die Depressivität war bei M2 signifikant reduziert (Reduktion der BDI-II und HAMD-17 Skores); und das signifikant stärker in der PA (HAMD-17). Kognition und Exzitabilität zeigten keine Änderung. Die in M1 verminderte Plastizität normalisierte sich in M2 in der PA, nicht aber in der CI. Neuroplastizität und BDI-II Skores in M1 korrelierten; und je deutlicher der BDI Skore abnahm, desto klarer war die Zunahme der Plastizität in M2. Dies stellt die Relevanz von plastizitätsinduzierenden Interventionen in der Depressionstherapie heraus

Physical exercise and unipolar depression. Effects on cognition, neuroplasticity, depression and coordinative movement skills

Brüchle W, Schwarzer C, Koester D, Schack T, Schneider U, Rosenkranz K. Physical exercise and unipolar depression. Effects on cognition, neuroplasticity, depression and coordinative movement skills. Presented at the 12th CeBiTec Symposium: Big data in medicine and biotechnology, Bielefeld

Untersuchung der koordinativen Fähigkeiten für ein Bewegungstraining bei unipolarer Depression

Schwarzer C, Brüchle W, Koester D, Schack T, Schneider H-U, Rosenkranz K. Untersuchung der koordinativen Fähigkeiten für ein Bewegungstraining bei unipolarer Depression. Zeitschrift für Neuropsychologie. 2018;29(3):S 199

Intensity dependent effect of cognitive training on motor cortical plasticity and cognitive performance in humans

Intervention-induced neuroplastic changes within the motor or cognitive system have been shown in the human brain. While cognitive and motor brain areas are densely interconnected, it is unclear whether this interconnectivity allows for a shared susceptibility to neuroplastic changes. Using the preparation for a theoretical exam as training intervention that primarily engages the cognitive system, we tested the hypothesis whether neuroplasticity acts across interconnected brain areas by investigating the effect on excitability and synaptic plasticity in the motor cortex. 39 healthy students (23 female) underwent 4 weeks of cognitive training while revision time, physical activity, concentration, fatigue, sleep quality and stress were monitored. Before and after cognitive training, cognitive performance was evaluated, as well as motor excitability using transcranial magnetic stimulation and long-term-potentiation-like (LTP-like) plasticity using paired-associative-stimulation (PAS). Cognitive training ranged individually from 1 to 7 h/day and enhanced attention and verbal working memory. While motor excitability did not change, LTP-like plasticity increased in an intensity-depending manner: the longer the daily revision time, the smaller the increase of neuroplasticity, and vice versa. This effect was not influenced by physical activity, concentration, fatigue, sleep quality or stress. Motor cortical plasticity is strengthened by a behavioural intervention that primarily engages cognitive brain areas. We suggest that this effect is due to an enhanced susceptibility to LTP-like plasticity, probably induced by heterosynaptic activity that modulates postsynaptic excitability in motorcortical neurones. The smaller increase of PAS efficiency with higher cognitive training intensity suggests a mechanism that balances and stabilises the susceptibility for synaptic potentiation

Physical Activity Reduces Clinical Symptoms and Restores Neuroplasticity in Major Depression

Brüchle W, Schwarzer C, Berns C, et al. Physical Activity Reduces Clinical Symptoms and Restores Neuroplasticity in Major Depression. Frontiers in Psychiatry. 2021;12.Major depressive disorder (MDD) is the most common mental disorder and deficits in neuroplasticity are discussed as one pathophysiological mechanism. Physical activity (PA) enhances neuroplasticity in healthy subjects and improves clinical symptoms of MDD. However, it is unclear whether this clinical effect of PA is due to restoring deficient neuroplasticity in MDD. We investigated the effect of a 3-week PA program applied on clinical symptoms, motor excitability and plasticity, and on cognition in patients with MDD (N= 23), in comparison to a control intervention (CI;N= 18). Before and after the interventions, the clinical symptom severity was tested using self- (BDI-II) and investigator- (HAMD-17) rated scales, transcranial magnetic stimulation (TMS) protocols were used to test motor excitability and paired-associative stimulation (PAS) to test long-term-potentiation (LTP)-like plasticity. Additionally, cognitive functions such as attention, working memory and executive functions were tested. After the interventions, the BDI-II and HAMD-17 decreased significantly in both groups, but the decrease in HAMD-17 was significantly stronger in the PA group. Cognition did not change notably in either group. Motor excitability did not differ between the groups and remained unchanged by either intervention. Baseline levels of LTP-like plasticity in the motor cortex were low in both groups (PA: 113.40 ± 2.55%; CI: 116.83 ± 3.70%) and increased significantly after PA (155.06 ± 10.48%) but not after CI (122.01 ± 4.1%). Higher baseline BDI-II scores were correlated with lower levels of neuroplasticity. Importantly, the more the BDI-II score decreased during the interventions, the stronger did neuroplasticity increase. The latter effect was particularly strong after PA (r= −0.835;p< 0.001). The level of neuroplasticity related specifically to the psychological/affective items, which are tested predominantly in the BDI-II. However, the significant clinical difference in the intervention effects was shown in the HAMD-17 which focuses more on somatic/neurovegetative items known to improve earlier in the course of MDD. In summary, PA improved symptoms of MDD and restored the deficient neuroplasticity. Importantly, both changes were strongly related on the individual patients' level, highlighting the key role of neuroplasticity in the pathophysiology and the clinical relevance of neuroplasticity-enhancing interventions for the treatment of MDD