Evidence map›Paper›PMID 32853175›Full record

ReviewAging2020

ATP synthase and Alzheimer's disease: putting a spin on the mitochondrial hypothesis.

Brad Ebanks, Thomas L Ingram, Lisa Chakrabarti

Open access · greenAbstract readReview
In one paragraph

Review in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  7. Open medicine (Warsaw, Poland) · 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

3 authors at 1 institution in 1 country.

Brad EbanksSchool of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington LE12 5RD, UK.
Thomas L IngramSchool of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington LE12 5RD, UK.
Lisa ChakrabartiSchool of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington LE12 5RD, UK.
University of Nottingham · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J014508/1
6 · The paper itself

Abstract

It is estimated that over 44 million people across the globe have dementia, and half of these cases are believed to be Alzheimer's disease (AD). As the proportion of the global population which is over the age 60 increases so will the number of individuals living with AD. This will result in ever-increasing demands on healthcare systems and the economy. AD can be either sporadic or familial, but both present with similar pathobiology and symptoms. Three prominent theories about the cause of AD are the amyloid, tau and mitochondrial hypotheses. The mitochondrial hypothesis focuses on mitochondrial dysfunction in AD, however little attention has been given to the potential dysfunction of the mitochondrial ATP synthase in AD. ATP synthase is a proton pump which harnesses the chemical potential energy of the proton gradient across the inner mitochondrial membrane (IMM), generated by the electron transport chain (ETC), in order to produce the cellular energy currency ATP. This review presents the evidence accumulated so far that demonstrates dysfunction of ATP synthase in AD, before highlighting two potential pharmacological interventions which may modulate ATP synthase.

Indexed as

Energy MetabolismAlzheimer DiseaseAnimalsBenzofuransBrainCurcuminDepsidesHumansMitochondriaMitochondrial Proton-Translocating ATPasesNeuroprotective AgentsBenzofuransCurcuminDepsidesJ147Mitochondrial Proton-Translocating ATPasesNeuroprotective Agentssalvianolic acid BAlzheimer's diseaseATP synthasemitochondria

Identifiers

PMID32853175
PMCPMC7485717
OpenAlexW3048288422

What OpenQuestion 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 OpenQuestion graph.