Evidence map›Paper›PMID 35048237›Full record

ReviewBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine2022

Mechanisms associated with the dysregulation of mitochondrial function due to lead exposure and possible implications on the development of Alzheimer's disease.

Lakshmi Jaya Madhuri Bandaru, Neelima Ayyalasomayajula, Lokesh Murumulla, Suresh Challa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Environmental toxins in neurodegeneration - a narrative review.Neurological research and practice · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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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

4 authors at 1 institution in 2 countries.

Lakshmi Jaya Madhuri BandaruDepartment of Cell Biology, National Institute of Nutrition, Indian Council of Medical Research (ICMR), Hyderabad, Telangana, 500007, India.ORCID 0000-0003-4393-7234
Neelima AyyalasomayajulaDepartment of Cell Biology, National Institute of Nutrition, Indian Council of Medical Research (ICMR), Hyderabad, Telangana, 500007, India.ORCID 0000-0002-5489-5925
Lokesh MurumullaDepartment of Cell Biology, National Institute of Nutrition, Indian Council of Medical Research (ICMR), Hyderabad, Telangana, 500007, India.
Suresh ChallaDepartment of Cell Biology, National Institute of Nutrition, Indian Council of Medical Research (ICMR), Hyderabad, Telangana, 500007, India. sureshnin2000@gmail.com.ORCID 0000-0002-7367-5848
Indian Council of Medical Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lead (Pb) is a multimedia contaminant with various pathophysiological consequences, including cognitive decline and neural abnormalities. Recent findings have reported an association of Pb toxicity with Alzheimer's disease (AD). Studies have revealed that mitochondrial dysfunction is a pathological characteristic of AD. According to toxicology reports, Pb promotes mitochondrial oxidative stress by lowering complex III activity in the electron transport chain, boosting reactive oxygen species formation, and reducing the cell's antioxidant defence system. Here, we review recent advances in the role of mitochondria in Pb-induced AD pathology, as well as the mechanisms associated with the mitochondrial dysfunction, such as the depolarisation of the mitochondrial membrane potential, mitochondrial permeability transition pore opening; mitochondrial biogenesis, bioenergetics and mitochondrial dynamics alterations; and mitophagy and apoptosis. We also discuss possible therapeutic options for mitochondrial-targeted neurodegenerative disease (AD).

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesAntioxidantsHumansLeadMitochondriaAmyloid beta-PeptidesAntioxidantsLeadAlzheimer’s diseaseLead toxicityMitochondrial dysfunctionReactive oxygen speciesβ-Amyloid peptide

Identifiers

PMID35048237
OpenAlexW4206663894

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.