Long term suppression of succinate dehydrogenase by selective inhibitor 3-nitropropionic acid has been used in rodents to model Huntington's disease where mitochondrial dysfunction and oxidative damages are primary pathological hallmarks for neuronal damage. Improvements in learning and memory abilities, recovery of energy levels, and reduction of excitotoxicity damage can be achieved through activation of Adenyl cyclase enzyme by a specific phytochemical forskolin. In this study, intraperitoneal administration of 10 mg/kg 3-nitropropionic acid for 15 days in rats notably reduced body weight, worsened motor cocordination (grip strength, beam crossing task, locomotor activity), resulted in learning and memory deficits, greatly increased acetylcholinesterase, lactate dehydrogenase, nitrite, and malondialdehyde levels, obviously decreased adenosine triphosphate, succinate dehydrogenase, superoxide dismutase, catalase, and reduced glutathione levels in the striatum, cortex and hippocampus. Intragastric administration of forskolin at 10, 20, 30 mg/kg dose-dependently reversed these behavioral, biochemical and pathological changes caused by 3-nitropropionic acid. These results suggest that forskolin exhibits neuroprotective effects on 3-nitropropionic acid-induced Huntington's disease-like neurodegeneration.

Alzheimer's disease is a severe neurodegenerative disorder that gradually results in loss of memory and impairment of cognitive functions in the elderly.Thedeposition of amyloid plaques is the primary event that leads to an oxidative and inflammatory reactions, neurofibrillary tangle formation, and ultimately neuronal death. The most prominent losses occur with cholinergic neurons that plays an important role in the formation of memory and cognitive functions. Insulin receptor numbers also altered, thusglucosemetabolism is defected in AD. Polyphenol ellagic acid (EA) possesses antioxidant, anti-inflammatory, anti-carcinogenic, anti-diabetic and cardioprotection activities.Activities of EA that are linked with protection of neuronal abnormalities like anti-depressant, antianxiety, anti-nociception. Ellagic acid inhibits β-secretase enzymatic activities, thus prevents the main pathologic hallmark of AD. There are varieties of herbal extracts and phytochemicals formulations extensively used to provide symptomatic relief to AD patients. Together these results our hypothesis that EA may prevent the neuronal dysfunctions as well as further work is also required to examine the pharmacological properties of EA in the protection of specially neurodegenerative disorder like AD. Here, we discuss how we can use the knowledge to improve treatment strategies of EA in AD and to explore the various signaling pathways involved in the progression of neuronal death.

No abstract

No abstract

No abstract