Neuroplasticity in Depressed Subjects Compared to Healthy Subjects

Yousefi, Khadijeh

Volume 29, Issue 10 (12-2022) RJMS 2022, 29(10): 452-461 | Back to browse issues page

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Yousefi K. Neuroplasticity in Depressed Subjects Compared to Healthy Subjects. RJMS 2022; 29 (10) :452-461
URL: http://rjms.iums.ac.ir/article-1-8268-en.html

Neuroplasticity in Depressed Subjects Compared to Healthy Subjects

Khadijeh Yousefi

Master's degree, Department of Psychology, South Tehran Branch, Islamic Azad University, Tehran, Iran. , yousefi.kh@hotmail.com

Abstract: (88 Views)

Background & Aims: Neurons communicate with each other using electrochemical signals. These signals are transmitted through a structure in the neuron called a synapse. Stimulating neural pathways through repetitive, memory-forming cognitive activity (such as studying or practicing) strengthens synaptic connections between neurons. In addition, the brain can create new synapses. While neural plasticity can occur naturally when experiencing different experiences, brain changes can also be activated through neuroplasticity exercises and cognitive training. Neuroplasticity refers to the structural and functional changes in the brain that occur due to new experiences. Because of the brain's plasticity, also called neuroplasticity, the brain can "rewire" and reorganize itself after a brain injury, as new connections are made and neural pathways terminate in the damaged brain areas. By studying cases of neural plasticity, researchers have found the relationship between neuroplasticity and depression to be similar to neuroplasticity and addiction. Depression can damage the brain by reinforcing unhealthy pathways. Researchers refer to these types of changes as "negative neuroplasticity". One of the goals of this article is to show that neuroplasticity interferes with depression.
Methods: This study was conducted using an objective test that is independent of the subject's effort and motivation, to compare neuroplasticity in 23 people with DSM-IV major depression and 23 healthy people of the same age and sex. The sample consisted of 23 depressed individuals (10 men, 13 women) who met DSM-IV criteria for a major depressive episode (20 with MDD, 3 with bipolar disorder) who were screened using the Structured Clinical Interview for DSM IV disorders. were evaluated. All were right-handed according to the Edinburgh Hand Questionnaire and participated after providing written informed consent (12). Severity of current depression was assessed using the Montgomery-Asberg Depression Rating Scale (MADRS; Montgomery & Asberg, 1979). Inclusion criteria were MADRS ⩾20 for MDD subjects and <6 for healthy subjects. In addition, depressed subjects should not have had a change in psychotropic medication dosage for at least 4 weeks prior to the study (6 weeks if starting new medication). Length of current depressive episode, treatment resistance (number of failed antidepressant drug trials), and current psychotropic medication were assessed in depressed subjects. Healthy control subjects had no previous history of depression and did not use psychotropic drugs. Other exclusion criteria included illicit drug use, alcohol abuse, musculoskeletal or neurological disorders, and electronic implants (13). During the same experimental day, subjects underwent blood sampling for BDNF genotyping and serum measurements (n = 36) (either DNA collected by buccal swab if they failed blood tests (n = 9) or failed all DNA tests ( n=1), were tested with the rotor pursuit test (to assess motor learning) and completed the PAS protocol 45 minutes later.
Results: Neuroplasticity in the motor cortex was evaluated using a brain stimulation pattern called paired association stimulation (PAS), which causes transient changes in motor cortex function. Excitability of the motor cortex before and after PAS was evaluated using single-pulse Transcranial magnetic stimulation (TMS) to induce motor-evoked potentials (MEPs) in the hand muscle. After PAS, MEP amplitude increased significantly in healthy subjects compared to depressed subjects (P=0.002). The functional significance of motor cortex changes was assessed using a motor learning task – a computerized version of the rotor pursuit task. Healthy controls also performed better in motor learning (P=0.02). Blood BDNF levels and genotype were assessed to determine any association with motor cortical plasticity.
Conclusion: This study demonstrated a significant deficit in neuroplasticity in depressed individuals compared to age- and sex-matched healthy individuals. This finding is significant as one of the first objective manifestations of neural vulnerability in depression. This study used a physiological measure of resilience that is not confounded by factors such as subjective rating and analysis, the subject's level of education, practice effects, or motivational factors, showing clear advantages compared to other cognitive or behavioral tests previously used to assess resilience. It was used in depression, it brings. There are three important limitations to this study. First, most depressed people were taking antidepressants. This is important because there is empirical evidence that antidepressants may affect neuroplasticity, although these studies have shown that they tend to increase rather than decrease plasticity (50). Further analysis of medicated and unmedicated depressed subjects found no differences in MEP changes after PAS between these groups, although both differed significantly from healthy controls. However, because the number of people who did not use psychoactive drugs was small, the study could not determine the extent to which the presence of drugs affected the results. Examining the results shows that the presence of antidepressants increases the variability in neuroplasticity measured in depressed subjects, which may confound the exploration of secondary outcomes, namely the relationship between neuroplasticity, motor learning and BDNF levels. A second limitation is that neuroplasticity was only measured once in the depressed group, and that was while they were symptomatic. A second measurement during recovery enables us to assess whether neural damage is a state or trait phenomenon and may help elucidate the underlying mechanisms. The suggestion that neural damage is a state phenomenon is supported by improvements in indirect measures of neuroplasticity, such as learning and memory, while patients are in recovery (44) as well as after antidepressant treatment in humans and in animal models Depression (39). A third limitation is that neuroplasticity was assessed in the motor cortex, which is not considered the primary site of brain dysfunction in depression. This study used the PAS protocol because it provides an accessible physiological measure of flexibility that is not confounded by factors such as subject motivation or prior learning and experience. Additionally, it supports other studies that have found abnormalities in motor cortex function in depressed individuals (40). It is possible that motor cortex abnormalities may reflect global pathophysiological disturbances in depression. However, PAS results were not correlated with motor learning, and did not seem related to BDNF measures. The importance of these results is that one of the first direct observations of reduced neuroplasticity in depressed individuals was provided using an objective test.

Keywords: Neuroplasticity, Major Depressive Disorder, Transcranial Magnetic Stimulation, Paired Association Stimulation, Motor Cortex, Motor Learning

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Type of Study: Research | Subject: Clinical Psychiatry