{"title":"TRP Channels as Emerging Therapeutic Targets in Neurological Disorders","authors":"A. Mazumder, Tanya Singh, V. Prabhakar, A. Kanda","doi":"10.25258/ijddt.13.1.70","DOIUrl":null,"url":null,"abstract":"Neurological disorders like Parkinson disease (PD), Alzheimer’s disease (AD), epilepsy, stroke, schizophrenia, depression, bipolar disorder, etc., are increasingly recognized as signifi cant causes of death and disability globally. All these neurological disorders have several similar causes, such as disturbance in Ca2+ homeostasis and misfolded proteins deposition in the brain through impairing the function of a no. of ion channels, including TRP channels. TRP channels superfamily consists of a broad collection of non-selective Ca2+ permeable channels that plays a crucial role in regulating intracellular Ca2+ homeostasis. These channels function as cellular sensors and are stimulated by a variety of physio-chemical stimulus, and endogenous and exogenous ligands. Numerous neuronal diseases are caused by disturbances in the activity of TRP channels, which are abundantly expressed in neuronal cells. When the activity of TRP channels is disturbed under pathological conditions, there is disruption of the homeostasis of neurons via oxidative stress, Ca2+ dyshomeostasis, and mitochondrial dysfunction. Therefore, these channels act as promising therapeutic candidates for pharmacological interventions in several neurological disorders. Thus within this review, we emphasize the function of TRP channels in neurological disorders and highlight the pharmacological modulators that target TRP channels","PeriodicalId":13851,"journal":{"name":"International Journal of Drug Delivery Technology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Drug Delivery Technology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.25258/ijddt.13.1.70","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0
Abstract
Neurological disorders like Parkinson disease (PD), Alzheimer’s disease (AD), epilepsy, stroke, schizophrenia, depression, bipolar disorder, etc., are increasingly recognized as signifi cant causes of death and disability globally. All these neurological disorders have several similar causes, such as disturbance in Ca2+ homeostasis and misfolded proteins deposition in the brain through impairing the function of a no. of ion channels, including TRP channels. TRP channels superfamily consists of a broad collection of non-selective Ca2+ permeable channels that plays a crucial role in regulating intracellular Ca2+ homeostasis. These channels function as cellular sensors and are stimulated by a variety of physio-chemical stimulus, and endogenous and exogenous ligands. Numerous neuronal diseases are caused by disturbances in the activity of TRP channels, which are abundantly expressed in neuronal cells. When the activity of TRP channels is disturbed under pathological conditions, there is disruption of the homeostasis of neurons via oxidative stress, Ca2+ dyshomeostasis, and mitochondrial dysfunction. Therefore, these channels act as promising therapeutic candidates for pharmacological interventions in several neurological disorders. Thus within this review, we emphasize the function of TRP channels in neurological disorders and highlight the pharmacological modulators that target TRP channels
期刊介绍:
International Journal of Drug Delivery Technology (IJDDT) provides the forum for reporting innovations, production methods, technologies, initiatives and the application of scientific knowledge to the aspects of pharmaceutics, including controlled drug release systems, drug targeting etc. in the form of expert forums, reviews, full research papers, and short communications.