Effect of amyloid beta (25-35) peptide on mitochondrial respiratiory function in neuroral cells over expressing ape1

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dc.contributor.authorKaur, Navrattam
dc.contributor.supervisorMantha, Anil K.
dc.date.accessioned2018-08-30T05:10:37Z
dc.date.accessioned2018-08-30T06:09:23Z
dc.date.accessioned2024-08-13T10:50:37Z
dc.date.available2018-08-30T05:10:37Z
dc.date.available2018-08-30T06:09:23Z
dc.date.available2024-08-13T10:50:37Z
dc.date.issued2014
dc.description.abstractAlzheimer's disease (AD) is an important public health problem which affects millions of people worldwide. The major pathological hallmarks associated with AD are the accumulation of amyloid beta (A?) in senile plaques and neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau proteins. Accumulating evidences point towards the role of oxidative stress and mitochondrial dysfunction in the pathogenesis of AD. Aging is considered as one of the greatest risk factor for AD. In order to maintain genome integrity, base excision repair (BER) pathway is the predominant pathway for repairing oxidized base lesions in neuronal cells. APE1 is the central enzyme of the BER-pathway, having both repair and redox activities and shown to enhance neuronal survival after oxidative stress. In my study, effect of A?(25-35) on mitochondrial ROS/RNS levels and activities of respiratory complexes (I, III, & IV) in neuronal cells was studied with and without ectopic APE1 expression and the neuro- modulatory role of Ginkgolide B (from leaves of G. biloba) was evaluated. It was seen that A?(25-35) increases the ROS/RNS levels in these cells which was decreased when pre-treated with Ginkgolide B (G.B) before treating with A?(25-35). APE1 levels were found to be decreased on treating with A?(25-35) and were increased on pre- treatment with G.B and subsequent treatment with A?(25-35). These results indicate that ectopic APE1 expression in the mitochondria of the neuronal cells might overcome the oxidative damage caused by A?(25-35). Also, phytochemical G.B has shown to modulate the mitochondrial complex activity upon A?(25-35)-induced oxidative stress and modulate the ROS/RNS levels in the presence of APE1. Further studies are needed to understand the mechanism of action of APE1 in relation to the above results, which will be carried out during my Ph.D. work.en_US
dc.identifier.accessionnoT00130
dc.identifier.citationKaur, Navrattan (2014) Effect of amyloid beta (25-35) peptide on mitochondrial respiratiory function in neuroral cells over expressing ape1.en_US
dc.identifier.urihttp://10.2.3.109/handle/32116/1740
dc.language.isoen_USen_US
dc.publisherCentral University of Punjaben_US
dc.subjectAlzheimer�s diseaseen_US
dc.subjectOxidative Stressen_US
dc.subjectAmyloid betaen_US
dc.subjectMitochondriaen_US
dc.subjectAPE1/Ref-1en_US
dc.subjectGinkgo bilobaen_US
dc.titleEffect of amyloid beta (25-35) peptide on mitochondrial respiratiory function in neuroral cells over expressing ape1en_US
dc.typeMphil Dissertationen_US

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