Evidence map›Paper›PMID 39808351›Full record

ArticleMetabolic brain disease2025

TeMac™ ameliorates memory impairment and cholinergic dysfunction in rats induced by scopolamine.

Bruno Dupon Akamba Ambamba, Fils Armand Ella, Dany Joël Ngassa Ngoumen, Janvier Aime Fotso Youovop, Guy Roussel Nguemto Takuissu, Ruth Edwige Kemadjou Dibacto, Martin Fonkoua, Damaris Enyegue Mandob, Sefirin Djiogue, Judith Laure Ngondi

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Network pharmacology, molecular docking andIBRO neuroscience reports · 2026
    Article
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

10 authors.

Bruno Dupon Akamba AmbambaDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Fils Armand EllaDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Dany Joël Ngassa NgoumenDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Janvier Aime Fotso YouovopDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Guy Roussel Nguemto TakuissuCentre for Food, Food Security and Nutrition Research, Institute of Medical Research and Medicinal Plant Studies, P. O. Box 13033, Yaounde, Cameroon.
Ruth Edwige Kemadjou DibactoDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Martin FonkouaDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Damaris Enyegue MandobDepartment of Biological Sciences, Higher Teacher's Training College, University of Yaoundé, P.O. Box 47, Yaounde, Cameroon.
Sefirin DjiogueDepartment of Animal Biology and Physiology, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon.
Judith Laure NgondiDepartment of Biochemistry, Faculty of Science, University of Yaoundé 1, P.O. Box 812, Yaounde, Cameroon. jlaurengondi@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is associated with cognitive impairments which are linked to a deficit in cholinergic function. The objective of this study was to evaluate the ability of TeMac™ to prevent memory impairment in scopolamine-rats model of Alzheimer's disease and by in silico approaches to identify molecules in TeMac™ inhibiting acetylcholinesterase. The cholinergic cognitive dysfunction was induced by intraperitoneal injection of scopolamine (1 mg/kg daily) in male Wistar rats for seven consecutive days. TeMac™ at 400 mg/kg body weight was orally administrated 60 min after scopolamine. Donepezil was used as a reference drug. The cognitive deficits were assessed by the Morris Water Maze and novel object recognition tests. After killing the rats, brains were immediately collected and used to carry out cholinesterase enzyme activity and histopathological analyses. Liquid chromatography-mass spectrometry (LC-MS) characterization of the TeMac™ was carried out and the identified molecules were tested in silico for their ability to cross the Blood-Brain Barrier (BBB) and inhibit acetylcholinesterase using molecular docking. The administration of the TeMac™ led to the prevention of memory deficits in rats by reducing significantly the cholinesterase enzymes activities and protecting against morphological alterations and loss of neurons in hippocampus. Seven major compounds were identified in TeMac™. Molecular docking simulations confirm the ability of oleaterminaloic acid B and stigmasterol to cross the BBB and interact with peripheral site and the acyl pocket of acetylcholinesterase. All these observations suggest that TeMac™ can therefore be used as an alternative for the management of AD-related cognitive impairments.

Indexed as

Cholinesterase InhibitorsMemory DisordersAcetylcholinesteraseAnimalsCognitive DysfunctionHippocampusMaleMaze LearningMolecular Docking SimulationRatsRats, WistarScopolamineAcetylcholinesteraseCholinesterase InhibitorsScopolamineAlzheimer's diseaseCholinergic dysfunctionMemory lossScopolamineTeMac™

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.