Evidence map›Paper›PMID 40423784›Full record

ArticlePsychopharmacology2025

Resveratrol mitigates activated astrocytes and microglia preventing Alzheimer's Disease (AD) progression and facilitates neuronal communication in Amyloid-β25-35 induced rat model for AD: A special emphasis on non-neuronal involvement in AD pathophysiology.

Kumar Surya, Anitha Rathinam, Meher Nisha Abubakkar, Kesavan Swaminathan Jayachandran, Mahesh Kandasamy, Muthuswamy Anusuyadevi

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Article in Psychopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

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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

6 authors.

Kumar SuryaMolecular Neurogerontology Laboratory, Department of Biochemistry, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620024, Tamil Nadu, India.
Anitha RathinamMolecular Neurogerontology Laboratory, Department of Biochemistry, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620024, Tamil Nadu, India.
Meher Nisha AbubakkarMolecular Neurogerontology Laboratory, Department of Biochemistry, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620024, Tamil Nadu, India.
Kesavan Swaminathan JayachandranMolecular Cardiology and Drug Discovery Laboratory, Department of Bioinformatics, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620024, Tamil Nadu, India.
Mahesh KandasamyLaboratory of Stem Cells and Neuroregeneration, Department of Animal Science, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620024, Tamil Nadu, India.
Muthuswamy AnusuyadeviMolecular Neurogerontology Laboratory, Department of Biochemistry, School of Life Sciences, Bharathidasan University, Tiruchirappalli, 620024, Tamil Nadu, India. janushyas@bdu.ac.in.ORCID http://orcid.org/0000-0003-0576-1776

Funding

Department of Science and Technology, Ministry of Science and Technology, India DST/CSRI/343GDepartment of Science and Technology, Ministry of Science and Technology, India DST WOS-A/LS-36/2020 (G)Indian Council of Medical Research 2019- 2605/CMB/Adhoc-BMSTamilnadu State Council For Science And Technology 2023BBC02012
6 · The paper itself

Abstract

rationaleAmyloid deposits initiate neuroinflammation by activating astrocytes and microglia in the hippocampus, increasing neuronal vulnerability and loss. Astrocytes, while essential for cerebral function, can contribute to neuronal dysfunction by retracting neuronal synapses, that forms a consequence of neuroinflammation, leading to cognitive deficits in Alzheimer's disease (AD). Upon Amyloid-β (Aβ) deposition, astrocytes become reactive as part of a repair mechanism, however this process can impair neurogenesis resulting in AD progression.

objectiveThe current study hypothesizes that resveratrol (RSV) can address inflammation and promote neural regeneration, mitigating cognitive decline. Our previous research highlights RSV's homeostatic effect through SIRT1 normalization, which is crucial in preventing AD progression. However, its neurogenic potential in AD remains underexplored.

methodsIn this study, Aβ25-35-induced AD rat model was used to study the anti-inflammatory, neurogenic and cellular homeostatic effect of RSV (30 mg/kg) for four weeks.

resultsResults showed increased Doublecortin expressing cells, indicating favorable neurogenesis in hippocampus. Immunofluorescence of microglia and astrocytes in the hippocampus revealed that RSV counteracted their activation by reducing the formation of engulfing microglia and elongated astrocytes. Behavioral assessments using the Morris water maze and cued radial arm maze demonstrated significant improvements in spatial and learning memory. These cognitive improvements were supported by increased choline acetyltransferase and SIRT1 levels.

conclusionThese findings suggest that RSV effectively reduces neuroinflammation, promotes neurogenesis in the sub granular zone of the hippocampus, and improves learning and memory in both control and AD conditions via SIRT1. This study highlights RSV's potential as a suitable therapeutic agent for AD.

Indexed as

Alzheimer DiseaseAstrocytesMicrogliaResveratrolAmyloid beta-PeptidesAnimalsDisease Models, AnimalDisease ProgressionDoublecortin ProteinHippocampusMaleNeurogenesisNeuronsPeptide FragmentsRatsRats, Sprague-DawleyAmyloid beta-Peptidesamyloid beta-protein (25-35)Doublecortin ProteinPeptide FragmentsResveratrolSirt1 protein, ratSirtuin 1Alzheimer's DiseaseHomeostasisNeurogenesisNeuroinflammationResveratrol

Identifiers

PMID40423784

What Socratic holds

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Registered trials

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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 Socratic graph.