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dc.contributor.authorOlloquequi, Jordi
dc.contributor.authorCano, Amanda
dc.contributor.authorSanchez-López, Elena
dc.contributor.authorCarrasco, Marina
dc.contributor.authorVerdaguer, Ester
dc.contributor.authorFortuna, Ana
dc.contributor.authorFolch, Jaume
dc.contributor.authorBulló, Mònica
dc.contributor.authorAuladell, Carme
dc.contributor.authorCamins, Antoni
dc.contributor.authorEttcheto, Miren
dc.date.accessioned2024-04-10T04:08:15Z
dc.date.available2024-04-10T04:08:15Z
dc.date.issued2022
dc.identifier10.1016/j.biopha.2022.113709
dc.identifier.issn07533322
dc.identifier.urihttps://hdl.handle.net/20.500.12728/10778
dc.description.abstractProtein 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. © 2022es_ES
dc.description.sponsorshipGeneralitat de Catalunya, (2014SGR‑525); Ministerio de Ciencia e Innovación, MICINN, (PID2021-123462OB-I00); Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED, (AARG-NTF-22-924702, CB06/05/2004)es_ES
dc.language.isoenes_ES
dc.publisherElsevier Masson s.r.l.es_ES
dc.subjectAlzheimer's diseasees_ES
dc.subjectInsulin receptores_ES
dc.subjectNeurodegenerative diseaseses_ES
dc.subjectNeuroinflammationes_ES
dc.subjectNeurological disorderses_ES
dc.subjectPTP1Bes_ES
dc.subjectType 2 diabeteses_ES
dc.titleProtein tyrosine phosphatase 1B (PTP1B) as a potential therapeutic target for neurological disorderses_ES
dc.typeArticlees_ES


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