Thalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in rats

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dc.authoridSalva, Emine/0000-0002-1159-5850
dc.authoridŞALVA, EMINE/0000-0002-1159-5850
dc.authoridAlan, Saadet/0000-0003-2329-151X
dc.authorwosidKARAN, Mehmet Akif/AAD-5304-2020
dc.authorwosidSalva, Emine/ABI-2766-2020
dc.authorwosidŞALVA, EMINE/CAH-3062-2022
dc.authorwosidAlan, Saadet/ABH-4282-2020
dc.contributor.authorElcioglu, H. K.
dc.contributor.authorKabasakal, L.
dc.contributor.authorAlan, S.
dc.contributor.authorSalva, E.
dc.contributor.authorTufan, F.
dc.contributor.authorKaran, M. A.
dc.date.accessioned2024-08-04T21:01:18Z
dc.date.available2024-08-04T21:01:18Z
dc.date.issued2013
dc.departmentİnönü Üniversitesien_US
dc.description.abstractNeuroinflammatory responses caused by amyloid beta (A beta) peptide deposits are involved in the pathogenesis of Alzheimer's disease (AD). Thalidomide has a significant anti-inflammatory effect by inhibiting TNF-alpha, which plays role in A beta neurotoxicity. We investigated the effect of thalidomide on AD-like cognitive deficits caused by intracerebroventricular injection of streptozotocin (STZ). Intraperitoneal thalidomide was administered 1 h before the first dose of STZ and continued for 21 days. Learning and memory behavior was evaluated on days 17, 18 and 19, and the rats were sacrificed on day 21 to examine histopathological changes. STZ injection caused a significant decrease in the mean escape latency in passive avoidance and decreased improvement of performance in Morris water maze tests. Histopathological changes were examined using hematoxylineosin and Bielschowsky staining. Brain sections of STZ treated rats showed increased neurodegeneration and disturbed linear arrangement of cells in the cortical area compared to controls. Thalidomide treatment attenuated significantly STZ induced cognitive impairment and histopathological changes. Thalidomide appears to provide neuroprotection from the memory deficits and neuronal damage induced by STZ.en_US
dc.description.sponsorshipMarmara University Scientific Research Community [SAG-D-300409-0114]en_US
dc.description.sponsorshipThis work was supported by The Marmara University Scientific Research Community (Project No: SAG-D-300409-0114, 2009).en_US
dc.identifier.doi10.3109/10520295.2012.744471
dc.identifier.endpage152en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue3-4en_US
dc.identifier.pmid23244235en_US
dc.identifier.startpage145en_US
dc.identifier.urihttps://doi.org/10.3109/10520295.2012.744471
dc.identifier.urihttps://hdl.handle.net/11616/104270
dc.identifier.volume88en_US
dc.identifier.wosWOS:000321904500004en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofBiotechnic & Histochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAlzheimeren_US
dc.subjectstreptozotocinen_US
dc.subjectthalidomideen_US
dc.titleThalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in ratsen_US
dc.typeArticleen_US

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