Evidence map›Paper›PMID 33998995›Full record

ArticleCurrent neuropharmacology2022

Mitochondrial Dysfunction in Alzheimer's Disease: Opportunities for Drug Development.

Shiveena Bhatia, Rishi Rawal, Pratibha Sharma, Tanveer Singh, Manjinder Singh, Varinder Singh

Open access · greenAbstract read
In one paragraph

Article in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

95 citing papers in PubMed, 154 citations in OpenAlex.

  1. Impact of multidomain lifestyle intervention on dynamics of cognitive frailty: post hoc analysis of the FINGER trial.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
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  12. Tubuloside B Alleviates AβNeurotoxicity research · 2026
    Article
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  15. Article
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  17. Review
  18. Article
  19. Open medicine (Warsaw, Poland) · 2026
    Article
  20. Review

35 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Shiveena BhatiaChitkara College of Pharmacy, Chitkara University, Punjab, India.
Rishi RawalSchool of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
Pratibha SharmaChitkara College of Pharmacy, Chitkara University, Punjab, India.
Tanveer SinghDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India.
Manjinder SinghChitkara College of Pharmacy, Chitkara University, Punjab, India.
Varinder SinghChitkara College of Pharmacy, Chitkara University, Punjab, India.
Chitkara University · INJamia Hamdard · INPunjabi University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the major reasons for 60-80% cases of senile dementia occurring as a result of the accumulation of plaques and tangles in the hippocampal and cortical neurons of the brain leading to neurodegeneration and cell death. The other pathological features of AD comprise abnormal microvasculature, network abnormalities, interneuronal dysfunction, increased β-amyloid production and reduced clearance, increased inflammatory response, elevated production of reactive oxygen species, impaired brain metabolism, hyperphosphorylation of tau, and disruption of acetylcholine signaling. Among all these pathologies, Mitochondrial Dysfunction (MD), regardless of it being an inciting insult or a consequence of the alterations, is related to all the associated AD pathologies. Observed altered mitochondrial morphology, distribution and movement, increased oxidative stress, dysregulation of enzymes involved in mitochondrial functioning, impaired brain metabolism, and impaired mitochondrial biogenesis in AD subjects suggest the involvement of mitochondrial malfunction in the progression of AD. Here, various pre-clinical and clinical evidence establishing MD as a key mediator in the progression of neurodegeneration in AD are reviewed and discussed with an aim to foster future MD based drug development research for the management of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesDrug DevelopmentHumansMitochondriaPlaque, AmyloidAmyloid beta-PeptidesAlzheimer’s diseaseapoptosismitochondrial dysfunctionoxidative stresstau proteinsβ-amyloid plaques

Identifiers

PMID33998995
PMCPMC9878959
OpenAlexW3160144137

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.