Autor según el artículo: Olloquequi, Jordi; Cano, Amanda; Sanchez-Lopez, Elena; Carrasco, Marina; Verdaguer, Ester; Fortuna, Ana; Folch, Jaume; Bullo, Monica; Auladell, Carme; Camins, Antoni; Ettcheto, Miren
Departamento: Bioquímica i Biotecnologia
Autor/es de la URV: Bulló Bonet, Mònica / Folch Lopez, Jaume
Palabras clave: Type 2 diabetes Ptp1b Neurological disorders Neuroinflammation Neurodegenerative diseases Insulin receptor Brain insulin-resistance Alzheimer’s disease Alzheimer's disease ursolic acid type 2 diabetes nigrostriatal tissue neurotrophic factor neurological disorders neuroinflammation neurodegenerative diseases liver-specific deletion insulin receptor improves neurobehavioral activity high-fat diet endoplasmic-reticulum stress cognitive deficits alzheimers-disease alzheimer ? s disease
Resumen: Protein tyrosine phosphatase 1B (PTP1B) is a typical member of the PTP family, considered a direct negative regulator of several receptor and receptor-associated tyrosine kinases. This widely localized enzyme has been involved in the pathophysiology of several diseases. More recently, PTP1B has attracted attention in the field of neuroscience, since its activation in brain cells can lead to schizophrenia-like behaviour deficits, anxiety-like effects, neurodegeneration, neuroinflammation and depression. Conversely, PTP1B inhibition has been shown to prevent microglial activation, thus exerting a potent anti-inflammatory effect and has also shown potential to increase the cognitive process through the stimulation of hippocampal insulin, leptin and BDNF/TrkB receptors. Notwithstanding, most research on the clinical efficacy of targeting PTP1B has been developed in the field of obesity and type 2 diabetes mellitus (TD2M). However, despite the link existing between these metabolic alterations and neurodegeneration, no clinical trials assessing the neurological advantages of PTP1B inhibition have been performed yet. Preclinical studies, though, have provided strong evidence that targeting PTP1B could allow to reach different pathophysiological mechanisms at once. herefore, specific interventions or trials should be designed to modulate PTP1B activity in brain, since it is a promising strategy to decelerate or prevent neurodegeneration in aged individuals, among other neurological diseases. The present paper fails to include all neurological conditions in which PTP1B could have a role; instead, it focuses on those which have been related to metabolic alterations and neurodegenerative processes. Moreover, only preclinical data is discussed, since clinical studies on the potential of PTP1B inhibition for treating neurological diseases are still required.Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Áreas temáticas: Saúde coletiva Química Pharmacology & pharmacy Pharmacology Odontología Medicine, research & experimental Medicine (miscellaneous) Medicina veterinaria Medicina iii Medicina ii Medicina i Materiais Interdisciplinar Farmacia Engenharias iii Engenharias ii Enfermagem Educação física Ciências biológicas iii Ciências biológicas ii Ciências biológicas i Ciências agrárias i Ciência de alimentos Ciência da computação Biotecnología Biodiversidade Astronomia / física
Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
Direcció de correo del autor: monica.bullo@urv.cat jaume.folch@urv.cat
Identificador del autor: 0000-0002-0218-7046 0000-0002-5051-8858
Fecha de alta del registro: 2024-10-12
Versión del articulo depositado: info:eu-repo/semantics/publishedVersion
URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
Referencia al articulo segun fuente origial: Biomedicine & Pharmacotherapy. 155 113709-113709
Referencia de l'ítem segons les normes APA: Olloquequi, Jordi; Cano, Amanda; Sanchez-Lopez, Elena; Carrasco, Marina; Verdaguer, Ester; Fortuna, Ana; Folch, Jaume; Bullo, Monica; Auladell, Carme; (2022). Protein tyrosine phosphatase 1B (PTP1B) as a potential therapeutic target for neurological disorders. Biomedicine & Pharmacotherapy, 155(), 113709-113709. DOI: 10.1016/j.biopha.2022.113709
Entidad: Universitat Rovira i Virgili
Año de publicación de la revista: 2022
Tipo de publicación: Journal Publications