Schizophrenia (SCZ) is a major debilitating, complex, and costly illness that strikes 1% of the world’s population. It is characterized by three general types of symptoms: Atypical symptoms (aggressiveness, agitation, delusions, hallucinations), depressive symptoms (alogia, avolition, anhedonia, apathy), and cognitive symptoms (impaired attention, learning, memory). The etiology of SCZ has still not been fully understood. Alteration in various neurochemical systems such as dopamine, serotonin, norepinephrine, gamma-aminobutyric acid, and glutamate are involved in the pathophysiology of SCZ. The lack of understanding regarding the exact pathogenic process may be the likely a reason for the non-availability of effective treatment, which can prevent onset and progression of the SCZ. The tools of modern neuroscience, drawing from neuroanatomy, neurophysiology, brain imaging, and psychopharmacology, promise to provide a host of new insights into the etiology and treatment of SCZ. In this review, we will discuss the role of the various neurotransmitter concerned and brain parts exaggerated in the SCZ.

Anxiety disorders are among the most common mental, emotional, and behavioral problems. These affect one-eighth of the total population worldwide. Anxiety disorders are a group of mental disorders characterized by irritability, fear, insomnia, nervousness, tachycardia, inability to concentrate, poor coping skills, palpitation, sweating, agoraphobia, and social withdrawal. Brain regions and networks involved in anxiety symptomatology is an effort to better understand the mechanism involved and to develop more effective treatments for the anxiety disorders. Thus, neuroanatomical and neuroimaging research in anxiety disorders has centered on the role of the amygdala, reciprocal connections between the amygdala and the prefrontal cortex, and, most recently, alterations in interoceptive processing by the anterior insula. Anxiety disorders are characterized by alterations in a diverse range of neurochemical systems, suggesting ample novel targets for drug therapies. The neurotransmitter like corticotropin-releasing factor, neuropeptides (substance P, neuropeptide Y, oxytocin, orexin, and galanin) are implicated in anxiety pathways. Each of these active areas of research holds promise for expanding and improving evidence-based treatment options for individuals suffering with clinical anxiety. Therefore, this article gives the information on the neurocognitive mechanisms, causes, neurotransmitter involved in anxiety disorders and emphasize on the therapeutic targets for anxiety disorders.

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Tourette’s syndrome (TS) is a neuropsychiatric and neurodevelopment disease typified by deterioration of motor and vocal tics which leads to neuropsychiatric symptoms and impaired motor activities manifestation. Several lines of study indicate the interplay of genetic and environmental factors to be involved in this complex neuropsychiatric syndrome. Approximately 1% people are affected worldwide from this syndrome. In this review, a concise outline presented on the classification, its clinical features and neuropsychiatric co-morbidities linked with this syndrome. This paper also highlights the neurochemistry, dysfunction of (Cortioc-Striato-Thalamo-Cortical) CSTC circuits in TS and an overview on the management approach towards the prevention of TS. Regardless of the major improvements in the understanding of exact cellular and molecular basis of TS, the various evidence indicate that the various neurotransmitter such as dopamine, glutamate, gamma- aminobutyric acid (GABA), serotonin, noradrenergic, cholinergic system, serotonergic system and histaminergic pathways play a major role in pathogenesis of TS. Several research indicates that the dysfunction of CSTS circuits occurred in this complex syndrome These areas of research have contributed to the therapeutic approach towards the management of TS and also provide the basis for future progress of the therapeutic strategies. Thus, tics generated in TS, which affect the social and academic life of patients and disruptive or troubling the family of patients. Patients existing with this syndrome have to face difficulties integrating into social life and coping with day to day basis activities, as a consequence of the syndrome.