Ascorbic acid ameliorates behavioural deficits and neuropathological alterations in rat model of Alzheimer’s disease

Olajide, Olayemi Joseph; Yawson, Emmanuel; Gbadamosi, Ismail Temitayo; Arogundade, Tolulope Timothy; Lambe, Ezra; Obasi, Kosisochukwu Kingsley; Lawal, Ismail Tayo; Ibrahim, A. A.; Ogunrinola, Kehinde Yomi

doi:10.1016/j.etap.2017.02.010

Cited by 67 publications

(43 citation statements)

References 54 publications

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“…while both brain regions were characterized by pyramidal soma with argentophilic masses, neuropil threads and dystrophic neurites in the PFC external pyramidal layer and CA3 pyramidal layer. Previous studies have also reported that aluminium toxicity induces corticohippocampal histopathologies such as chromatolysis (Olajide et al, 2017b), gliosis (Elizabeth et al, 2020), extensive neuronal cell loss (Akinola et al, 2015), neurofibrillary tangles (Kowall et al, 1989), and amyloid plaques (Rodella et al, 2008). Cumulatively, these findings have shown that aluminium induces Alzheimer-like histopathological changes in the brain of the experimental animals.…”

Section: Discussionmentioning

confidence: 98%

“…NIC has been shown to amyloidosis in experimental models of AD (Lahiri et al, 2002;Nordberg et al, 2002;Utsuki et al, 2002). AA potentiates its neuroprotection, primarily by acting as an antioxidant in its capacity (Covarrubias-Pinto et al, 2015;Foyer, 2017) enabling it to scavenge for reactive oxygen and nitrogen species (Du et al, 2012), reducing lipid peroxidation (Maggio et al, 2017), and ultimately sustaining the cellular integrity of the PFC and hippocampus (Olajide et al, 2017b).…”

Section: Discussionmentioning

confidence: 99%

“…Hence, NIC tendency to drive oxidative stress undermines its therapeutic advantages. AA is a potent antioxidant vitamin (Covarrubias-Pinto et al, 2015) whose deficiency had been linked to several neurodegenerative diseases (Olajide et al, 2017b;Parle and Dhingra, 2003). Owing to its antioxidant properties, dietary supplementation of AA has been associated with reduced prevalence and incidence of AD.…”

Section: Introductionmentioning

confidence: 99%

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Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Gbadamosi

Omotoso

2020

Preprint

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Alzheimer's disease is the most common cause of dementia and is hallmarked by β-amyloid plaque and neurofibrillary tangles deposition in the CNS. The complex mechanism that underlies AD pathogenesis has made the development of a definitive cure futile. Exploring the possible therapeutic advantages of combining two neuromodulatory molecules with different mechanisms of neuroprotection is an interesting way of drug discovery. Ascorbic acid (AA), a potent antioxidant molecule, and nicotine (NIC), an allosteric modulator of nAChRs, have both been documented to independently proffer neuroprotection in experimental and clinical neurodegenerative cases. This study elucidated the putative therapeutic advantages of combining ascorbic acid and nicotine as a treatment regimen against the aluminium induced anxiety, corticohippocampal histopathology and perturbed neuroenergetics in rats induced with Alzheimer-like neuropathology Rats treated with 100 mg/kg aluminium chloride for 28 days presented with significantly increased stretch attend posture frequency and centre square entry. Aluminium significantly depleted the activities of G6PDH while increasing lactate levels. Corticohippocampal histomorphology of these animals showed poor histoarchitecture, increased congophilic and argentophilic densities that were coupled with increased anti-NSE immunopositivity. Animals post-treated with NIC (10mg/kg) and AA (100mg/kg) for 28 days presented with reduced anxiety level and improved corticohippocampal histomorphology. AA normalized G6PDH and lactate levels while the congophilic density was reduced by NIC. Corticohippocampal argentophilic density anti-NSE immunopositivity were also normalized by AA+NIC. The findings from this study have shown that a combination of ascorbic acid and nicotine effectively mitigated aluminium-induced corticohippocampal neuropathology and perturbed neuroenergetics.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Gbadamosi

Omotoso

2020

Preprint

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“…Ascorbic acid, also known as vitamin C, has shown therapeutic benefits against AD-related pathological conditions in experimental animal studies. The mechanisms behind the beneficial effects include scavenging free radicals, inhibiting membrane lipid peroxidation, modulating neuronal bioenergetics, and antiproteolytic properties (Olajide et al, 2017). Moreover, it was reported that vitamin D supplementation improved the Mini-Mental State Exam (MMSE) score for cognitive impairments in AD (Annweiler, 2014).…”

Section: Diet and Disease Relationshipsmentioning

confidence: 99%

Nonpharmacological treatment options for Alzheimer’s disease: from animal testing to clinical studies

Türkez¹,

Arslan²,

Stefano³

et al. 2020

Turk J Zool

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Despite extensive pharmacological approaches, there is no curative therapy for Alzheimer's disease (AD) or other types of dementias. While current pharmacological options alleviate some symptoms of AD, they can lead to various adverse effects. Hence, nonpharmacological treatment options for AD are often considered with the assumption that they are safe, effective, and economic in managing patients. Furthermore, studies on animal models have suggested that environmental exposures like diet, music, or rewardrelated actions can stimulate neuronal regeneration and differentiation without using any pharmacological factors. The aim of this review is to provide a summary of nonpharmacological treatment options for the management of cognitive, emotional, and behavioral symptoms of AD. In addition, this review provides an overview of the challenging and encouraging experiences and recent studies and problems in cognitive training related to animal models. Nonpharmacological studies of AD are discussed in this literature review in terms of animal models, physical activity, brain stimulation, and the role of social communication.

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“…Very recently, Olajide et al examined the effects of ascorbic acid on behavioral and cortical and hippocampal neurochemical changes elicited by repeated administration of aluminum chloride (AlCl 3 ), a model of Alzheimer's disease, in rats. A 15‐day treatment with ascorbic acid (100 mg/kg daily) significantly decreased behavioral deficits in rats through inhibition of molecular and cellular stressor proteins activated by AlCl 3 .…”

Section: Role Of Ascorbic Acid In Neurodegenerative Diseasesmentioning

confidence: 99%

Preventive and therapeutic potential of ascorbic acid in neurodegenerative diseases

2017

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In this review, we summarize the involvement of ascorbic acid in neurodegenerative diseases by presenting available evidence on the behavioral and biochemical effects of this compound in animal models of neurodegeneration as well as the use of ascorbic acid as a therapeutic approach to alleviate neurodegenerative progression in clinical studies. Ascorbate, a reduced form of vitamin C, has gained interest for its multiple functions and mechanisms of action, contributing to the homeostasis of normal tissues and organs as well as to tissue regeneration. In the brain, ascorbate exerts neuromodulatory functions and scavenges reactive oxygen species generated during synaptic activity and neuronal metabolism. These are important properties as redox imbalance and abnormal protein aggregation constitute central mechanisms implicated in the pathogenesis of neurodegenerative diseases, including Alzheimer's, Parkinson's, and Huntington's diseases, multiple sclerosis, and amyotrophic lateral sclerosis. Indeed, several studies have indicated an association between low serum ascorbate concentrations and neurodegeneration. Moreover, ascorbic acid is a suitable candidate for supplying either antioxidant defense or modulation of neuronal and astrocytic metabolism under neurodegenerative conditions. Ascorbic acid acts mainly by decreasing oxidative stress and reducing the formation of protein aggregates, which may contribute to the reduction of cognitive and/or motor impairments observed in neurodegenerative processes. Although several studies support a possible role of ascorbic acid administration against neurodegeneration, more researches are essential to substantiate the existing results and accelerate the knowledge in this field.

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Ascorbic acid ameliorates behavioural deficits and neuropathological alterations in rat model of Alzheimer’s disease

Cited by 67 publications

References 54 publications

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Corticohippocampal Neuroenergetics and histomorphology in aluminium-induced neurotoxicity: Putative therapeutic roles of ascorbic acid and nicotine

Nonpharmacological treatment options for Alzheimer’s disease: from animal testing to clinical studies

Preventive and therapeutic potential of ascorbic acid in neurodegenerative diseases

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