Evidence map›Paper›PMID 39827052›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2025

Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.

Kyle C McGill Percy, Zunren Liu, Xin Qi

Abstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–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

34 citing papers in PubMed.

  1. Review
  2. Review
  3. Metabolic Shifts Precede Cognitive Decline in the Male hAß-KI Alzheimer's Mouse Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. ACS omega · 2026
    Article
  16. Article
  17. Article
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  19. Review
  20. Review
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

3 authors.

Kyle C McGill PercyDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Zunren LiuDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Xin QiDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Center for Mitochondrial Research and Therapeutics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: xxq38@case.edu.

Funding

Mechanism of white matter pathology in Alzheimer's diseaseR01AG076051 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI XIN QI · 2022 to 2026
$3.0M
Role of brain lipid metabolism in Alzheimer's diseaseR01AG065240 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI QI, XIN · 2020 to 2024
$3.0M
Proteostasis dysregulation and alpha-synucleinR01NS115903 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI QI, XIN · 2020 to 2023
$2.4M
Regulation of CHCHD6 in Alzheimer's diseaseRF1AG074346 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI QI, XIN · 2022 to 2022
$2.1M
NIA NIH HHS R01 AG065240NIA NIH HHS R01 AG076051NIA NIH HHS RF1 AG074346NINDS NIH HHS R01 NS115903
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by progressive neurodegeneration, marked by the accumulation of amyloid-β (Aβ) plaques and tau tangles. Emerging evidence suggests that mitochondrial dysfunction plays a pivotal role in AD pathogenesis, driven by impairments in mitochondrial quality control (MQC) mechanisms. MQC is crucial for maintaining mitochondrial integrity through processes such as proteostasis, mitochondrial dynamics, mitophagy, and precise communication with other subcellular organelles. In AD, disruptions in these processes lead to bioenergetic failure, gene dysregulation, the accumulation of damaged mitochondria, neuroinflammation, and lipid homeostasis impairment, further exacerbating neurodegeneration. This review elucidates the molecular pathways involved in MQC and their pathological relevance in AD, highlighting recent discoveries related to mitochondrial mechanisms underlying neurodegeneration. Furthermore, we explore potential therapeutic strategies targeting mitochondrial dysfunction, including gene therapy and pharmacological interventions, offering new avenues for slowing AD progression. The complex interplay between mitochondrial health and neurodegeneration underscores the need for innovative approaches to restore mitochondrial function and mitigate the onset and progression of AD.

Indexed as

Alzheimer DiseaseMitochondriaMitochondrial DiseasesAnimalsGenetic TherapyHumansMitophagyMolecular Targeted TherapyAlzheimer's diseaseAmyloid betaGene therapyMitochondrial quality controlPharmacotherapyTauopathy

Identifiers

PMID39827052
PMCPMC12047401

What OpenQuestion holds

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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.