Evidence map›Paper›PMID 38006469›Full record

ReviewMolecular neurobiology2024

Environmental Toxins and Alzheimer's Disease: a Comprehensive Analysis of Pathogenic Mechanisms and Therapeutic Modulation.

Rishika Dhapola, Prajjwal Sharma, Sneha Kumari, Jasvinder Singh Bhatti, Dibbanti HariKrishnaReddy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  20. The Epidemiological and Toxicological Intersection of Air Pollution and Dementia.Reviews of environmental contamination and toxicology · 2025
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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

5 authors at 1 institution in 1 country.

Rishika DhapolaAdvanced Pharmacology and Neuroscience Laboratory, Department of Pharmacology, Central University of Punjab, Bathinda, 151 401, India.
Prajjwal SharmaAdvanced Pharmacology and Neuroscience Laboratory, Department of Pharmacology, Central University of Punjab, Bathinda, 151 401, India.
Sneha KumariAdvanced Pharmacology and Neuroscience Laboratory, Department of Pharmacology, Central University of Punjab, Bathinda, 151 401, India.
Jasvinder Singh BhattiLaboratory of Translational Medicine and Nanotherapeutics, Department of Human Genetics and Molecular Medicine, Central University of Punjab, Bathinda, 151 401, India.
Dibbanti HariKrishnaReddyAdvanced Pharmacology and Neuroscience Laboratory, Department of Pharmacology, Central University of Punjab, Bathinda, 151 401, India. harikrishnareddy0011@gmail.com.ORCID http://orcid.org/0000-0003-2616-0195
Central University of Punjab · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is a leading cause of mortality worldwide. Inorganic and organic hazards, susceptibility to harmful metals, pesticides, agrochemicals, and air pollution are major environmental concerns. As merely 5% of AD cases are directly inherited indicating that these environmental factors play a major role in disease development. Long-term exposure to environmental toxins is believed to progress neuropathology, which leads to the development of AD. Numerous in-vitro and in-vivo studies have suggested the harmful impact of environmental toxins at cellular and molecular level. Common mechanisms involved in the toxicity of these environmental pollutants include oxidative stress, neuroinflammation, mitochondrial dysfunction, abnormal tau, and APP processing. Increased expression of GSK-3β, BACE-1, TNF-α, and pro-apoptotic molecules like caspases is observed upon exposure to these environmental toxins. In addition, the expression of neurotrophins like BDNF and GAP-43 have been found to be reduced as a result of toxicity. Further, modulation of signaling pathways involving PARP-1, PGC-1α, and MAPK/ERK induced by toxins have been reported to contribute in AD pathogenesis. These pathways are a promising target for developing novel AD therapeutics. Drugs like epigallocatechin-gallate, neflamapimod, salsalate, dexmedetomidine, and atabecestat are in different phases of clinical trials targeting the pathways for possible treatment of AD. This review aims to culminate the correlation between environmental toxicants and AD development. We emphasized upon the signaling pathways involved in the progression of the disease and the therapeutics under clinical trial targeting the altered pathways for possible treatment of AD.

Indexed as

Alzheimer DiseaseAnimalsEnvironmental PollutantsHumansEnvironmental PollutantsAlzheimer’s diseaseEnvironmental pollutantsHeavy metalsMAPK/ERKPARPSIRT1

Identifiers

PMID38006469
OpenAlexW4389002717

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.