Evidence map›Paper›PMID 34433343›Full record

ReviewAnnals of medicine2021

Role of neurotoxicants in the pathogenesis of Alzheimer's disease: a mechanistic insight.

Fatema Yasmin Nisa, Md Atiar Rahman, Md Amjad Hossen, Mohammad Forhad Khan, Md Asif Nadim Khan, Mumtahina Majid, Farjana Sultana, Md Areeful Haque

Open access · goldAbstract readReview
In one paragraph

Review in Annals of medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
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

14 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Neuroprotective properties ofIBRO neuroscience reports · 2026
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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

8 authors at 2 institutions in 2 countries.

Fatema Yasmin NisaDepartment of Biochemistry and Molecular Biology, Faculty of Biological Sciences, University of Chittagong, Chittagong, Bangladesh.
Md Atiar RahmanDepartment of Biochemistry and Molecular Biology, Faculty of Biological Sciences, University of Chittagong, Chittagong, Bangladesh.
Md Amjad HossenDepartment of Pharmacy, International Islamic University Chittagong, Chittagong, Bangladesh.
Mohammad Forhad KhanDepartment of Pharmacy, International Islamic University Chittagong, Chittagong, Bangladesh.
Md Asif Nadim KhanDepartment of Biochemistry and Molecular Biology, Faculty of Biological Sciences, University of Chittagong, Chittagong, Bangladesh.
Mumtahina MajidDepartment of Biochemistry and Molecular Biology, Faculty of Biological Sciences, University of Chittagong, Chittagong, Bangladesh.
Farjana SultanaDepartment of Biochemistry and Molecular Biology, Faculty of Biological Sciences, University of Chittagong, Chittagong, Bangladesh.
Md Areeful HaqueDepartment of Pharmacy, International Islamic University Chittagong, Chittagong, Bangladesh.ORCID 0000-0003-2935-6345
University of Chittagong · BDInternational Islamic University Chittagong · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most conspicuous chronic neurodegenerative syndrome, which has become a significant challenge for the global healthcare system. Multiple studies have corroborated a clear association of neurotoxicants with AD pathogenicity, such as Amyloid beta (Aβ) proteins and neurofibrillary tangles (NFTs), signalling pathway modifications, cellular stress, cognitive dysfunctions, neuronal apoptosis, neuroinflammation, epigenetic modification, and so on. This review, therefore, aimed to address several essential mechanisms and signalling cascades, including Wnt (wingless and int.) signalling pathway, autophagy, mammalian target of rapamycin (mTOR), protein kinase C (PKC) signalling cascades, cellular redox status, energy metabolism, glutamatergic neurotransmissions, immune cell stimulations (e.g. microglia, astrocytes) as well as an amyloid precursor protein (APP), presenilin-1 (PSEN1), presenilin-2 (PSEN2) and other AD-related gene expressions that have been pretentious and modulated by the various neurotoxicants. This review concluded that neurotoxicants play a momentous role in developing AD through modulating various signalling cascades. Nevertheless, comprehension of this risk agent-induced neurotoxicity is far too little. More in-depth epidemiological and systematic investigations are needed to understand the potential mechanisms better to address these neurotoxicants and improve approaches to their risk exposure that aid in AD pathogenesis.Key messagesInevitable cascade mechanisms of how Alzheimer's Disease-related (AD-related) gene expressions are modulated by neurotoxicants have been discussed.Involvement of the neurotoxicants-induced pathways caused an extended risk of AD is explicited.Integration of cell culture, animals and population-based analysis on the clinical severity of AD is addressed.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAutophagyFemaleHumansMaleMetalsMiddle AgedNeuroinflammatory DiseasesOxidative StressAmyloid beta-PeptidesAmyloid beta-Protein PrecursorMetalsAlzheimer’s diseaseneurodegenerationNeurotoxicantsoxidative stresstoxic metals

Identifiers

PMID34433343
PMCPMC8405119
OpenAlexW3194955543

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.