<![CDATA[Central Nervous System Agents in Medicinal Chemistry (Volume 24 - Issue 1)]]> https://www.benthamscience.com/journal/36 RSS Feed for Journals | BenthamScience EurekaSelect (+https://www.benthamscience.com) 2024-03-25 <![CDATA[Central Nervous System Agents in Medicinal Chemistry (Volume 24 - Issue 1)]]> https://www.benthamscience.com/journal/36 <![CDATA[Evolving New Forms of Treatment]]>https://www.benthamscience.com/article/1390022024-03-25 <![CDATA[Bridging the Mind and Gut: Uncovering the Intricacies of Neurotransmitters, Neuropeptides, and their Influence on Neuropsychiatric Disorders]]>https://www.benthamscience.com/article/1376972024-03-25Background: The gut-brain axis (GBA) is a bidirectional signaling channel that facilitates communication between the gastrointestinal tract and the brain. Recent research on the gut-brain axis demonstrates that this connection enables the brain to influence gut function, which in turn influences the brain and its cognitive functioning. It is well established that malfunctioning of this axis adversely affects both systems' ability to operate effectively.

Objective: Dysfunctions in the GBA have been associated with disorders of gut motility and permeability, intestinal inflammation, indigestion, constipation, diarrhea, IBS, and IBD, as well as neuropsychiatric and neurodegenerative disorders like depression, anxiety, schizophrenia, autism, Alzheimer's, and Parkinson's disease. Multiple research initiatives have shown that the gut microbiota, in particular, plays a crucial role in the GBA by participating in the regulation of a number of key neurochemicals that are known to have significant effects on the mental and physical well-being of an individual.

Methods: Several studies have investigated the relationship between neuropsychiatric disorders and imbalances or disturbances in the metabolism of neurochemicals, often leading to concomitant gastrointestinal issues and modifications in gut flora composition. The interaction between neurological diseases and gut microbiota has been a focal point within this research. The novel therapeutic interventions in neuropsychiatric conditions involving interventions such as probiotics, prebiotics, and dietary modifications are outlined in this review.

Results: The findings of multiple studies carried out on mice show that modulating and monitoring gut microbiota can help treat symptoms of such diseases, which raises the possibility of the use of probiotics, prebiotics, and even dietary changes as part of a new treatment strategy for neuropsychiatric disorders and their symptoms.

Conclusion: The bidirectional communication between the gut and the brain through the gut-brain axis has revealed profound implications for both gastrointestinal and neurological health. Malfunctions in this axis have been connected to a range of disorders affecting gut function as well as cognitive and neuropsychiatric well-being. The emerging understanding of the role of gut microbiota in regulating key neurochemicals opens up possibilities for novel treatment approaches for conditions like depression, anxiety, and neurodegenerative diseases.

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<![CDATA[Glutamate Receptors and C-ABL Inhibitors: A New Therapeutic Approach for Parkinson's Disease]]>https://www.benthamscience.com/article/1374252024-03-25 <![CDATA[A Comprehensive Review on Potential Molecular Drug Targets for the Management of Alzheimer's Disease]]>https://www.benthamscience.com/article/1373142024-03-25 <![CDATA[GABA-transaminase: A Key Player and Potential Therapeutic Target for Neurological Disorders]]>https://www.benthamscience.com/article/1373002024-03-25via GABA-T overstimulation or inhibition would play a vital role in the pathogenesis of various neurological disorders. This review emphasizes the leading participation of GABA-T in neurological disorders like Huntington's disease, epilepsy, autism, Alzheimer's disease, and multiple sclerosis. In Huntington's disease, epilepsy, and multiple sclerosis, the surfeited performance of GABA-T results in diminished levels of GABA, whereas in autism, the subsidence of GABA-T activity causes the elevation in GABA contents, which is responsible for behavioral changes in these disorders. Therefore, GABA-T inhibitors (in Huntington's disease, epilepsy, and multiple sclerosis) or agonists (in autism) can be used therapeutically. In the context of Alzheimer's disease, some researchers favor the stimulation of GABA-T activity whereas some disagree with it. Therefore, the activity of GABA-T concerning Alzheimer's disease is still unclear. In this way, studies of GABA-T enzymatic activity in contrast to neurological disorders could be undertaken to understand and be considered a therapeutic target for several GABA-ergic CNS diseases.]]> <![CDATA[Molecular Pathway, Epidemiological Data and Treatment Strategies of Fungal Infection (Mycoses): A Comprehensive Review]]>https://www.benthamscience.com/article/1374272024-03-25 <![CDATA[Sulfonamide Derivatives: Recent Compounds with Potent Anti-alzheimer’s Disease Activity]]>https://www.benthamscience.com/article/1377652024-03-25