Please use this identifier to cite or link to this item: http://13.232.72.61:8080/jspui/handle/123456789/3981
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dc.contributor.authorS, Maya-
dc.date.accessioned2020-12-16T05:38:20Z-
dc.date.available2020-12-16T05:38:20Z-
dc.date.issued2018-12-
dc.identifier.citationhttp://lrc.acharyainstitutes.in:8080/jspui/handle/123456789/777en_US
dc.identifier.urihttp://13.232.72.61:8080/jspui/handle/123456789/3981-
dc.description.abstractAmyotrophic lateral sclerosis (ALS) is a progressive, fatal, multisystemic neurodegenerative disease with evidence of motor neuron loss in the brain and spinal cord. The factors behind the ALS are genetic, oxidative stress, glutamate excitotoxicity, protein aggregation, apoptosis, autoimmunity, production of inflammatory cytokines, alteration in a cellular process, metabolic impairment, mitochondrial damage, glial activation, and disruption in axonal transport. The multiple pathogeneses behind the development and progression of ALS make a challenge to find out an effective therapy for this disease. This study aims to unravel the mechanisms behind the neuroprotective effects of wedelolactone and gallic acid against aluminium-induced neurodegeneration and thereby to unlock a platform to find a cure for sALS.en_US
dc.publisherRGUHSen_US
dc.subjectALS; Wedelolactone; Gallic acid; Neuroprotection; Neurodegeneration; Aluminium-induced toxicity; Quinolinic acid-induced toxicity; Glutamate toxicity; Motor learning; Motor coordinationen_US
dc.titleEvaluation of Neuroprotective Activity of Wedelolactone and Gallic Acid on the Pathogenesis of Amyotrophic Lateral Sclerosisen_US
dc.typeThesisen_US
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