Contemporary Perspectives on Neurobiology and Treatment of Tic Disorders: A Narrative Review

Epilepsy as a Multiscale Network Disorder: Integrating Precision Therapeutics and Emerging Experimental Platforms

Epilepsy is increasingly recognized as a multiscale network disorder rather than solely a condition of neuronal hyperexcitability, and the coordinated use of complementary human-relevant platforms may help incorporate multiscale mechanistic insights into therapeutic development and evaluation, narrow persistent translational gaps, and support more predictive and mechanism-informed treatment strategies.

Pharmacological Insights in to Schizophrenia: Neurochemical Dysregulation, Disease Mechanisms and Future Therapeutic Strategies

Schizophrenia is a chronic and heterogeneous neuropsychiatric condition that affects approximately one percent of the global population and is associated with substantial impairments in perception, cognition, emotional regulation, and social functioning. The disorder typically manifests during late adolescence or early adulthood and arises from a complex interaction between genetic susceptibility and environmental influences acting during critical stages of brain development. Clinically, schizophrenia is characterized by three major symptom clusters: positive symptoms, including hallucinations, delusions, and disorganized thinking; negative symptoms, such as reduced motivation, emotional blunting, social withdrawal, and diminished pleasure; and cognitive deficits involving attention, memory, learning, and executive processing. Traditional dopamine-centered theories primarily explain the emergence of positive symptoms but fail to adequately account for persistent negative and cognitive impairments. Contemporary research highlights the involvement of glutamatergic dysregulation, particularly N-methyl-D-aspartate receptor hypofunction, altered serotonergic signaling, and disrupted cortico–striatal–thalamic connectivity. Neuroimaging studies further demonstrate widespread structural and functional brain abnormalities, supporting a neurodevelopmental basis for the disorder. Increasing evidence also implicates neuroinflammatory processes, immune imbalance, and oxidative stress in the progression of neuronal dysfunction and white matter damage. Although currently available antipsychotic medications effectively alleviate positive symptoms in many patients, their clinical benefit is limited by adverse effects and insufficient efficacy against negative and cognitive domains. These limitations emphasize the necessity for safer and more comprehensive therapeutic strategies. This review summarizes current understanding of the clinical features, etiological factors, biological mechanisms, and pharmacological management of schizophrenia, while outlining emerging therapeutic targets that may guide future research and drug development.

New Insights in the Management of Esophageal Disorders of Gut-Brain Interaction

Towards precision psychiatry: initial foundations and future directions.

Neuroplasticity in Major Depressive Disorder: A Systematic Review of Current Insights and Treatment Implications

Major Depressive Disorder (MDD) is associated with impaired Neuroplasticity, which may be essential in understanding the neuroplastic mechanisms underlying MDD in order to improve diagnosis and treatment strategies. This review helps in the synthesis of evidence from recent studies exploring cortical excitability, biomarkers of treatment response, molecular modulation, and structural Neuroplasticity in depression. Findings show that individuals with MDD may exhibit altered cortical inhibition and facilitation compared to healthy controls, with evidence of impaired plasticity in the dorsolateral prefrontal cortex (DLPFC). Neuroplasticity-based measures, such as Transcranial Magnetic Stimulation TMS- evoked potentials, gamma power modulation, and Repetitive Transcranial Magnetic Stimulation rTMS-induced functional connectivity, show potential for treatment prediction. Pharmacological studies highlight serotonergic and noradrenergic modulation roles in enhancing plasticity, while ketamine-induced changes and magnetic seizure therapy provide insights into adaptations in Neuroplasticity. Structural studies reveal hippocampal and cortical thickness alterations, while behavioural interventions like exercise may promote neurocognitive benefits linking to Neuroplasticity. Collectively, the evidence underscores the multifaceted role of Neuroplasticity in MDD and the treatment implications.

Neuroprogression in substance use disorders: Integrating molecular mechanisms, brain circuitry, biomarkers, and implications for clinical staging and service design.

Substance use disorders (SUDs) are increasingly recognised as neuroprogressive conditions characterised by cumulative and dynamic alterations across multiple levels of brain organisation. This integrative narrative review synthesises current evidence on the molecular, cellular, circuit-level, and biomarker mechanisms underlying neuroprogression in SUDs and proposes a multilevel translational framework. Evidence from preclinical and clinical studies indicates that chronic exposure to psychoactive substances induces persistent neuroinflammation, oxidative stress, mitochondrial dysfunction, and epigenetic dysregulation, which collectively disrupt synaptic plasticity and promote ferroptotic processes. These alterations progressively translate into large-scale dysfunction of frontolimbic and frontostriatal circuits, contributing to impaired inhibitory control, maladaptive decision making, and increased vulnerability to relapse. Neuroimaging findings further support this model by demonstrating structural, functional, and metabolic changes associated with chronic substance use. In parallel, neurofilament light chain has emerged as a promising but non-specific research fluid biomarker of cumulative neuroaxonal damage, with potential value for linking biological alterations and clinical expression in future longitudinal and multimodal studies. From a translational perspective, this framework may inform early intervention, clinical staging, and the development of more integrated and scalable models of care. Overall, neuroprogression provides a coherent model for understanding SUDs and may contribute to guiding more precise, biologically informed approaches in addiction psychiatry.