Evidence map›Paper›PMID 32339611›Full record

ReviewExperimental neurology2020

Mitochondria in Alzheimer's disease and their potential role in Alzheimer's proteostasis.

Ian W Weidling, Russell H Swerdlow

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
8.1field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Unveiling the pathogenesis and therapeutic strategies of Alzheimer's disease through cuproptosis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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12 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

2 authors at 1 institution in 1 country.

Ian W WeidlingUniversity of Kansas Alzheimer's Disease Center, University of Kansas Medical Center, Kansas City, KS, USA.
Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Center, University of Kansas Medical Center, Kansas City, KS, USA. Electronic address: rswerdlow@kumc.edu.
University of Kansas Medical Center · US

Funding

University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JEFFREY Murray BURNS, RUSSELL H. SWERDLOW · 2021 to 2026
$25.3M
University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
Validation and Mechanistic Interrogation of Metabolism Targeting for ADR01AG060733 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SULLIVAN, DEBRA K, SWERDLOW, RUSSELL H. · 2019 to 2024
$3.5M
Mechanistic Basis of the mtDNA Haplogroup J-Alzheimer's Disease AssociationR01AG061194 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2019 to 2023
$1.9M
NIA NIH HHS P30 AG035982NIA NIH HHS P30 AG072973NIA NIH HHS R01 AG060733NIA NIH HHS R01 AG061194
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive brain disorder characterized by memory loss and the accumulation of two insoluble protein aggregates, tau neurofibrillary tangles and beta-amyloid plaques. Widespread mitochondrial dysfunction also occurs and mitochondria from AD patients display changes in number, ultrastructure, and enzyme activities. Mitochondrial dysfunction in AD presumably links in some way to its other disease characteristics, either as a cause or consequence. This review characterizes AD-associated mitochondrial perturbations and considers their position in its pathologic hierarchy. It focuses on the crosstalk that occurs between mitochondria, nuclear gene expression, and cytosolic signaling pathways that serves to maintain cell homeostasis. To this point, recent evidence indicates mitochondria trigger retrograde responses that influence cell proteostasis in general and AD proteostasis specifically. Potentially pertinent retrograde responses include the mitochondrial unfolded protein response (mtUPR), integrated stress response (ISR), autophagy/mitophagy, and proteasome function. A fuller perspective of mitochondrial dysfunction in AD, and its relation to protein aggregation, could enhance our overall understanding of this disease.

Indexed as

Alzheimer DiseaseAnimalsHumansMitochondriaProteostasisAggregationAlzheimer's diseaseMetabolismMitochondriaMitochondrial DNAMitophagyProteostasis

Identifiers

PMID32339611
PMCPMC7282957
OpenAlexW3017698458

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.