Abstract
Currently prescribed medications for the treatment of Alzheimer’s disease (AD) that are based on acetylcholinesterase inhibition only offer symptomatic relief but do not provide protection against neurodegeneration. There appear to be an intense need for the development of therapeutic strategies that not only improve brain functions but also prevent neurodegeneration. The oxidative stress is one of the main causative factors of AD. Various antioxidants are being investigated to prevent neurodegeneration in AD. The objective of this study was to investigate the neuroprotective effects of naringenin (NAR) against AlCl3+D-gal induced AD-like symptoms in an animal model. Rats were orally pre-treated with NAR (50 mg/kg) for two weeks and then exposed to AlCl3+D-gal (150 mg/kg + 300 mg/kg) intraperitoneally for one week to develop AD-like symptoms. The standard drug, donepezil (DPZ) was used as a stimulator of cholinergic activity. Our results showed that NAR pre-treatment significantly protected AD-like behavioral disturbances in rats. In DPZ group, rats showed improved cognitive and cholinergic functions but the neuropsychiatric functions were not completely improved and showed marked histopathological alterations. However, NAR not only prevented AlCl3+D-gal induced AD-like symptoms but also significantly prevented neuropsychiatric dysfunctions in rats. Results of present study suggest that NAR may play a role in enhancing neuroprotective and cognition functions and it can potentially be considered as a neuroprotective compound for therapeutic management of AD in the future.
Highlights
Alzheimer’s disease (AD) is a neuronal degenerative disease and is one of the most financially draining diseases to the society [1]
NAR pre-treatment in AD-like model rats significantly increased (p
The present study suggests that NAR, a potent antioxidant, has an ability to prevent oxidative damage by increasing neuronal antioxidant enzyme activities, preventing lipid peroxidation (LPO) and stimulating cholinergic, serotonergic, and dopaminergic neurotransmission (Fig 12)
Summary
Alzheimer’s disease (AD) is a neuronal degenerative disease and is one of the most financially draining diseases to the society [1]. Short-term memory (STM) impairment is generally the first clinical sign of AD [5] and studies have reported that such neurodegenerative mechanisms are under the influence of oxidative stress [6, 7]. Accumulation of intracellular τ protein in the form of neurofibrillary tangles is extensively reported as pathological hallmark in AD and it is suggested that accumulation of plaques and tangles are mainly initiated and expedited by oxidative stress [9]. If free radicals are not quickly removed, their accumulation may result in cellular senescence [11]. These presumptions demonstrate the effectiveness of antioxidant therapy in particular cases
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