Evidence mapPaperPMID 39254911Full record

ReviewMolecular neurobiology2025

Exploring the Mechanisms and Therapeutic Approaches of Mitochondrial Dysfunction in Alzheimer's Disease: An Educational Literature Review.

Mostafa Hossam El Din Moawad, Ibrahim Serag, Ibraheem M Alkhawaldeh, Abdallah Abbas, Abdulrahman Sharaf, Sumaya Alsalah, Mohammed Ahmed Sadeq, Mahmoud Mohamed Mohamed Shalaby, Mahmoud Tarek Hefnawy, Mohamed Abouzid and 1 more

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Boosting Neurogenesis as a Strategy in Treating Alzheimer's Disease.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. 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

11 authors.

Mostafa Hossam El Din MoawadFaculty of Pharmacy, Clinical Department, Alexandria Main University Hospital, Alexandria, Egypt.
Ibrahim SeragFaculty of Medicine, Mansoura University, Mansoura, Egypt. Ibrahimserag@std.mans.edu.eg.
Ibraheem M AlkhawaldehFaculty of Medicine, Mutah University, Al-Karak, Jordan.
Abdallah AbbasFaculty of Medicine, Al-Azhar University, Damietta, Egypt.
Abdulrahman SharafDepartment of Clinical Pharmacy, Salmaniya Medical Complex, Government Hospital, Manama, Bahrain.
Sumaya AlsalahMinistry of Health, Primary Care, Governmental Health Centers, Manama, Bahrain.
Mohammed Ahmed SadeqMisr University for Science and Technology, 6th of October City, Egypt.
Mahmoud Mohamed Mohamed ShalabyFaculty of Medicine, Ain Shams University, Cairo, Egypt.
Mahmoud Tarek HefnawyFaculty of Medicine, Zagazig University, Zagazig, Egypt.
Mohamed AbouzidDepartment of Physical Pharmacy and Pharmacokinetics, Faculty of Pharmacy, Poznan University of Medical Sciences, Rokietnicka 3 St., 60-806, Poznan, Poland. mmahmoud@ump.edu.pl.
Mostafa MeshrefDepartment of Neurology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) presents a significant challenge to global health. It is characterized by progressive cognitive deterioration and increased rates of morbidity and mortality among older adults. Among the various pathophysiologies of AD, mitochondrial dysfunction, encompassing conditions such as increased reactive oxygen production, dysregulated calcium homeostasis, and impaired mitochondrial dynamics, plays a pivotal role. This review comprehensively investigates the mechanisms of mitochondrial dysfunction in AD, focusing on aspects such as glucose metabolism impairment, mitochondrial bioenergetics, calcium signaling, protein tau and amyloid-beta-associated synapse dysfunction, mitophagy, aging, inflammation, mitochondrial DNA, mitochondria-localized microRNAs, genetics, hormones, and the electron transport chain and Krebs cycle. While lecanemab is the only FDA-approved medication to treat AD, we explore various therapeutic modalities for mitigating mitochondrial dysfunction in AD, including antioxidant drugs, antidiabetic agents, acetylcholinesterase inhibitors (FDA-approved to manage symptoms), nutritional supplements, natural products, phenylpropanoids, vaccines, exercise, and other potential treatments.

Indexed as

Alzheimer DiseaseMitochondriaAnimalsHumansAlzheimer’s DiseaseMitochondrial DysfunctionTherapeutic Modalities

Identifiers

PMID39254911
PMCPMC12078384

What Socratic 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 Socratic graph.