Evidence map›Paper›PMID 40450332›Full record

ReviewEuropean journal of medical research2025

The role of mitochondrial dysfunction in the pathogenesis of Alzheimer's disease and future strategies for targeted therapy.

Xin Li, Ziyang Wu, Xiaying Si, Jing Li, Guode Wu, Manxia Wang

Abstract readReview
In one paragraph

Review in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

6 authors.

Xin LiDepartment of Neurology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Ziyang WuThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Xiaying SiDepartment of Psychiatry, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Jing LiDepartment of Neurology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Guode WuDepartment of Neurology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Manxia WangDepartment of Neurology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China. wmx322@aliyun.com.

Funding

Cuiying Scientific and Technological Innovation Program of The Second Hospital & Clinical Medical School, Lanzhou University, China CY2022-MS-A07Cuiying Scientific Training Program for Undergraduates of The Second Hospital & Clinical Medical School, Lanzhou University, China CYXZ2023-46Natural Science Foundation of Gansu Province, China 22JR5RA994Natural Science Foundation of Gansu Province, China 23JRRA0961
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, behavioral impairments, and psychiatric comorbidities. The pathogenesis of AD remains incompletely elucidated, despite advances in dominant hypotheses such as the β-amyloid (Aβ) cascade, tauopathy, cholinergic deficiency, and neuroinflammation mechanisms. However, these hypotheses inadequately explain the multifactorial nature of AD, which exposes limitations in our understanding of its mechanisms. Mitochondrial dysfunction is known to play a pivotal role in AD, and since patients exhibit intracellular mitochondrial dysfunction and structural changes in the brain at an early stage, correcting the imbalance of mitochondrial homeostasis and the cytopathological changes caused by it may be a potential target for early treatment of AD. Mitochondrial structural abnormalities accelerate AD pathogenesis. For instance, structural and functional alterations in the mitochondria-associated endoplasmic reticulum membrane (MAM) can disrupt intracellular Ca

Indexed as

Alzheimer DiseaseMitochondriaAmyloid beta-PeptidesAnimalsHumansMitochondrial DynamicsMolecular Targeted Therapytau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseMitochondrial dynamicsMitochondrial quality controlMitophagyTherapeutic targets

Identifiers

PMID40450332
PMCPMC12125765

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.