Evidence map›Paper›PMID 41503898›Full record

ArticleCurrent Alzheimer research2026

Effect of Ascorbic Acid on the Transgenic

Yasir Hasan Siddique, Gulshan Ara, Falaq Naz, Himanshi Varshney, Kajal Gaur, Iqra Subhan, Javeria Fatima, Smita Jyoti

Abstract read
PubMed Publisher
In one paragraph

Article in Current Alzheimer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Yasir Hasan SiddiqueLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Gulshan AraLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Falaq NazLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Himanshi VarshneyLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Kajal GaurLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Iqra SubhanLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Javeria FatimaLaboratory of Alternative Animal Models, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, Uttar Pradesh, India.
Smita JyotiDepartment of Zoology, School of Sciences, IFTM, Moradabad, Uttar Pradesh, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by extracellular accumulation of amyloid-beta (Aβ) peptides, particularly the toxic Aβ42 isoform. Aβ42 aggregation induces excessive reactive oxygen species (ROS) production, resulting in oxidative damage, lipid peroxidation, protein oxidation, and neuronal dysfunction. Oxidative stress plays a pivotal role in AD pathogenesis, making antioxidants promising therapeutic candidates.

objectiveThe present study aimed to evaluate the neuroprotective efficacy of ascorbic acid (AA), a potent dietary antioxidant, in a transgenic Drosophila melanogaster model of AD expressing human Aβ42 in neuronal tissues. MATERIALS AND

methodsTransgenic Drosophila melanogaster expressing human Aβ42 under a neuronal driver were used as the AD model, with wild-type flies as controls. Flies were supplemented with optimized, non-toxic doses of AA throughout their lifespan. Oxidative stress and antioxidant defense were assessed using glutathione (GSH) levels, glutathione S-transferase (GST), thiobarbituric acid-reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), protein carbonyl content (PCC), and acetylcholinesterase (AChE) activity. Locomotor performance was evaluated using the negative geotaxis assay.

resultsAA supplementation significantly restored redox homeostasis by increasing GSH levels and reducing TBARS and PCC. Antioxidant enzyme activities (GST, SOD, and CAT) were normalized, accompanied by partial restoration of AChE activity. AA-fed AD flies exhibited improved locomotor performance, delayed cognitive decline, and extended lifespan compared to untreated AD flies. DISCUSSION: The findings indicate that AA mitigates Aβ42-induced oxidative stress by enhancing endogenous antioxidant defenses and reducing oxidative damage. The improvement in AChE activity suggests preservation of cholinergic neurotransmission, which is crucial for learning and memory. Behavioral recovery and lifespan extension further demonstrate the systemic neuroprotective effects of AA, supporting its role as a multifunctional modulator of AD-associated pathology.

conclusionThis study highlights the multidimensional neuroprotective potential of ascorbic acid in a transgenic Drosophila AD model. By alleviating oxidative stress, preserving cholinergic function, improving behavior, and promoting longevity, AA emerges as a promising, low-cost antioxidant for further evaluation in higher animal models and clinical settings.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAntioxidantsAscorbic AcidNeuronsNeuroprotective AgentsPeptide FragmentsAcetylcholinesteraseAnimalsAnimals, Genetically ModifiedDisease Models, AnimalDrosophila melanogasterGlutathioneGlutathione TransferaseHumansOxidative StressAcetylcholinesteraseAmyloid beta-Peptidesamyloid beta-protein (1-42)AntioxidantsAscorbic AcidGlutathioneGlutathione TransferaseNeuroprotective AgentsPeptide FragmentsSuperoxide DismutaseAscorbic acidcognitive.Drosophilahuman Aβ42neuronsoxidative stress

Identifiers

PMID41503898

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.