Cited by 79Alzheimer's disease research and treatmentsAluminum toxicity and tolerance in plants and animalsMedicinal Plants and Neuroprotection

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

Olajide, Olayemi Joseph, Yawson, Emmanuel Olusola, Gbadamosi, Ismail Temitayo, Arogundade, Tolulope Timothy, Lambe, Ezra, Obasi, Kosisochukwu, Lawal, Ismail Tayo, Ibrahim, Abdulmumin +1 more·2017·Environmental Toxicology and Pharmacology

Abstract

Exploring the links between neural pathobiology and behavioural deficits in Alzheimer's disease (AD), and investigating substances with known therapeutic advantages over subcellular mechanisms underlying these dysfunctions could advance the development of potent therapeutic molecules for AD treatment. Here we investigated the efficacy of ascorbic acid (AA) in reversing aluminium chloride (AlCl 3)-induced behavioural deficits and neurotoxic cascades within prefrontal cortex (PFC) and hippocampus of rats. A group of rats administered oral AlCl 3 (100mg/kg) daily for 15days showed degenerative changes characterised by significant weight loss, reduced exploratory/working memory, frontal-dependent motor deficits, cognitive decline, memory dysfunction and anxiety during behavioural assessments compared to control. Subsequent analysis showed that oxidative impairment-indicated by depleted superoxide dismutase and lipid peroxidation (related to glutathione-S-transferase activity), cholinergic deficits seen by increased neural acetylcholinesterase (AChE) expression and elevated lactate dehydrogenase underlie behavioural alterations. Furthermore, evidences of proteolysis were seen by reduced Nissl profiles in neuronal axons and dendrites which correspond to apoptotic changes observed in H&E staining of PFC and hippocampal sections. Interestingly, AA (100mg/kg daily for 15days) significantly attenuated behavioural deficits in rats through inhibition of molecular and cellular stressor proteins activated by AlCl 3. Our results showed that the primary mechanisms underlying AA therapeutic advantages relates closely with its abilities to scavenge free radicals, prevent membrane lipid peroxidation, modulate neuronal bioenergetics, act as AChE inhibitor and through its anti-proteolytic properties. These findings suggest that supplementing endogenous AA capacity through its pharmacological intake may inhibit progression of AD-related neurodegenerative processes and behavioural alterations.

Integrity signals

Registry

Crossref · 10.1016/j.etap.2017.02.010

Cites

63 of 63 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Many molecules, including lignans, flavonoids, tannins, polyphenols, triterpenes, sterols, and alkaloids, have been shown to have anti-inflammatory, anti-amyloidogenic, and anticholinesterase properties.

    “Many molecules, including lignans, flavonoids, tannins, polyphenols, triterpenes, sterols, and alkaloids, have been shown to have anti-inflammatory, anti-amyloidogenic, anticholinesterase, and anti-inflammatory properties.”

    From An update on the novel and approved drugs for Alzheimer disease (2022) · cites this paper as Olajide et al., 2017

Cites

1 retracted

Flagged first, then by citations

1 of the 64 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Olajide, O. J., Yawson, E. O., Gbadamosi, I. T., Arogundade, T. T., Lambe, E., Obasi, K., Lawal, I. T., Ibrahim, A., & Ogunrinola, K. Y.
Affiliations
University of Ilorin (NG)
Corresponding author
Olajide, Olayemi Joseph
Venue
Environmental Toxicology and Pharmacology
Publisher
Elsevier BV
Published
2017-03
Volume
50
Pages
200-211
ISSN
1382-6689 (ISSN-L)
OpenAlex
W2587096908
Cited by
79
References
64
Citations by year
2026: 5 · 2025: 6 · 2024: 8 · 2023: 6 · 2022: 12 · 2021: 11 · 2020: 16 · 2019: 5 · 2018: 2 · 2017: 8
FWCI
6.29
Type
journal article
Language
en
Open access
closed
Locations
  • Environmental Toxicology and Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Olajide Oluwamayokun Oluwatomiyosi for taking time to proofread this manuscript
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Aluminum toxicity and tolerance in plants and animals
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
vitamin C, Alzheimer's disease, aluminum chloride-induced neurotoxicity, behavioural deficits, prefrontal cortex, hippocampus, oxidative stress, lipid peroxidation, acetylcholinesterase, cholinergic deficit, apoptosis, proteolysis, memory impairment, anxiety, neuroprotection
MeSH terms
Aluminum Chloride, Alzheimer Disease, Animals, Anxiety, Ascorbic Acid, Chlorides, Disease Models, Animal, Exploratory Behavior, Hippocampus, Humans, Lipid Peroxidation, Prefrontal Cortex, Aluminum Compounds, Disease Progression, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review