Articles

The gut-brain axis (GBA) has emerged as a central focus in the study of neurodevelopmental disorders, particularly autism spectrum disorder (ASD). Research suggests that microbial composition and its metabolic byproducts influence neural development, synaptic plasticity, and behavior [1,2,3]. A structured bibliometric analysis of Scopus and Web of Science records was performed using Bibliometrix and VOSviewer to trace trends and thematic evolution of GBA–ASD literature [7,8]. In parallel, a data-driven pathway modeling approach maps microbial metabolites (e.g., short-chain fatty acids, tryptophan catabolites) to host signaling pathways including vagal stimulation, immune cytokine modulation, and blood–brain barrier (BBB) permeability [4,5]. Simulations implemented in Python’s NetworkX illustrate how perturbations in metabolite flux may influence CNS outcomes. The findings reveal growing emphasis on butyrate, serotonin, microglial priming, and maternal immune activation in ASD-related GBA studies, and highlight the need for rigorous empirical validation of computational predictions [9,10,11].

Major depressive disorder is characterized, among other symptoms, by depressed mood and anhedonia associated with a high rate of suicidal ideation. In recent years, research has shown reduced expression of the brain-derived neurotrophic factor (BDNF) in limbic areas of individuals with depression. This reduction of BDNF is reversed by antidepressants in animal models of stress. Stress is one of the main triggers of mood disorders such as depression. Also, administration of BDNF increases the number of serotonergic fibers and serotonergic innervation, indicating an increase of serotonin in the synaptic cleft by this neurotrophin. Thus, BDNF appears to be one of the targets of antidepressant drugs for the increase of monoamines and remission of symptoms of major depression. The purpose of this review was to show the evidence that indicates BDNF as a molecular substrate for vulnerability to depression and the response of this substrate to the antidepressants.