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dc.contributor.authorYildiz-Unal, Aysegul
dc.contributor.authorKorulu, Sirin
dc.contributor.authorKarabay, Arzu
dc.date.accessioned2020-11-20T16:17:37Z
dc.date.available2020-11-20T16:17:37Z
dc.date.issued2015
dc.identifier.issn1178-2021
dc.identifier.urihttps://doi.org/10.2147/NDT.S78226
dc.identifier.urihttps://hdl.handle.net/20.500.12809/3279
dc.descriptionKarabay, Arzu/0000-0001-5150-5349; Yildiz Unal, Aysegul/0000-0001-6356-7459; Korulu, Sirin/0000-0001-6762-0659en_US
dc.descriptionWOS: 000348987000001en_US
dc.descriptionPubMed ID: 25709452en_US
dc.description.abstractCalpains are calcium-dependent proteolytic enzymes that have deleterious effects on neurons upon their pathological over-activation. According to the results of numerous studies to date, there is no doubt that abnormal calpain activation triggers activation and progression of apoptotic processes in neurodegeneration, leading to neuronal death. Thus, it is very crucial to unravel all the aspects of calpain-mediated neurodegeneration in order to protect neurons through eliminating or at least minimizing its lethal effects. Protecting neurons against calpain-activated apoptosis basically requires developing effective, reliable, and most importantly, therapeutically applicable approaches to succeed. From this aspect, the most significant studies focusing on preventing calpain-mediated neurodegeneration include blocking the N-methyl-D-aspartate (NMDA)-type glutamate receptor activities, which are closely related to calpain activation; directly inhibiting calpain itself via intrinsic or synthetic calpain inhibitors, or inhibiting its downstream processes; and utilizing the neuroprotectant steroid hormone estrogen and its receptors. In this review, the most remarkable neuroprotective strategies for calpain-mediated neurodegeneration are categorized and summarized with respect to their advantages and disadvantages over one another, in terms of their efficiency and applicability as a therapeutic regimen in the treatment of neurodegenerative diseases.en_US
dc.description.sponsorshipTurkish Academy of Sciences Distinguished Young Scientist Award (TUBA-GEBIP)Turkish Academy of Sciences; Scientific and Technological Research Council of Turkey (TUBITAK)-The Basic Sciences Research Group (TBAG)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [108T811]en_US
dc.description.sponsorshipThe "Speedy/RINGO over-expression to prevent calpain-mediated apoptosis" study was funded by grants to Arzu Karabay from The Turkish Academy of Sciences Distinguished Young Scientist Award (TUBA-GEBIP) and The Scientific and Technological Research Council of Turkey (TUBITAK)-The Basic Sciences Research Group (TBAG) (grant number 108T811).en_US
dc.item-language.isoengen_US
dc.publisherDove Medical Press Ltden_US
dc.item-rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCalpainen_US
dc.subjectNeurodegenerationen_US
dc.subjectNeuroprotectionen_US
dc.subjectCalpain Inhibitorsen_US
dc.subjectNMDARen_US
dc.subjectSpeedy/RINGOen_US
dc.titleNeuroprotective strategies against calpain-mediated neurodegenerationen_US
dc.item-typereviewen_US
dc.contributor.departmenten_US
dc.contributor.departmentTemp[Yildiz-Unal, Aysegul] Mugla Sitki Kocman Univ, Fac Sci, Dept Mol Biol & Genet, TR-48000 Kotekli, Mugla, Turkey -- [Korulu, Sirin] Istanbul Arel Univ, Dept Mol Biol & Genet, Istanbul, Turkey -- [Karabay, Arzu] Istanbul Tech Univ, Dept Mol Biol & Genet, Fac Sci & Letters, TR-80626 Istanbul, Turkeyen_US
dc.identifier.doi10.2147/NDT.S78226
dc.identifier.volume11en_US
dc.identifier.startpage297en_US
dc.identifier.endpage310en_US
dc.relation.journalNeuropsychiatric Disease and Treatmenten_US
dc.relation.publicationcategoryDiğeren_US


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