Evidence map›Paper›PMID 42527552›Full record

ArticleNature neuroscience2026

Mitochondrial accumulation and lysosomal dysfunction result in mitochondrial plaques in Alzheimer's disease.

Xiuli Dan, Deborah L Croteau, Wenlong Liu, Xixia Chu, Ross A McDevitt, Paul D Robbins, Vilhelm A Bohr

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Xiuli DanSection on DNA Repair, National Institute on Aging, NIH, Baltimore, MD, USA.
Deborah L CroteauSection on DNA Repair, National Institute on Aging, NIH, Baltimore, MD, USA.
Wenlong LiuLaboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, MD, USA.
Xixia ChuSection on DNA Repair, National Institute on Aging, NIH, Baltimore, MD, USA.
Ross A McDevittComparative Medicine Section, National Institute on Aging, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-3722-9047
Paul D RobbinsDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Institute on the Biology of Aging and Metabolism, University of Minnesota, Minneapolis, MN, USA. probbins@umn.edu.ORCID http://orcid.org/0000-0003-1068-7099
Vilhelm A BohrSection on DNA Repair, National Institute on Aging, NIH, Baltimore, MD, USA. vbohr@sund.ku.dk.ORCID http://orcid.org/0000-0003-4823-6429

Funding

U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) U19 AG056278 and U54 AG079754
6 · The paper itself

Abstract

Dysfunctional mitophagy is proposed as a key component of Alzheimer's disease (AD) pathology, yet direct in vivo evidence and mechanistic insights are still lacking. Here we show that AD model mice expressing a mitophagy reporter (APP/PSEN1/mt-Keima) develop large accumulation of acidic and neutral mitochondria within neuronal processes that form a previously unrecognized pathological structure termed mitochondrial plaques (MPs). The development of MPs is driven by abnormal mitochondrial buildup and lysosomal recruitment occurs as a delayed response to promote mitochondrial degradation. However, degradation through mitophagy is incomplete due to impaired lysosomal functions, resulting in accumulation of both neutral and acidic mitochondria. MPs frequently codevelop with amyloid to form mixed plaques but can also emerge independently at early stages of disease. Notably, MPs were also identified in the 5xFAD AD mouse model and postmortem human AD brains. These findings establish MPs as a new pathological entity in AD.

Indexed as

Alzheimer DiseaseLysosomesMitochondriaPlaque, AmyloidAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalHumansMiceMice, TransgenicMitophagyNeuronsPresenilin-1Amyloid beta-Protein PrecursorPresenilin-1

Identifiers

PMID42527552

What Socratic 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 Socratic graph.