Evidence map›Paper›PMID 31309927›Full record

ArticleeLife2019

Expression of WIPI2B counteracts age-related decline in autophagosome biogenesis in neurons.

Andrea Kh Stavoe, Pallavi P Gopal, Andrea Gubas, Sharon A Tooze, Erika Lf Holzbaur

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
6.9field-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

60 citing papers in PubMed, 80 citations in OpenAlex.

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  17. Monitoring Autophagy in Human Aging: Key Cell Models and Insights.Frontiers in bioscience (Landmark edition) · 2025
    Review
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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

5 authors at 2 institutions in 2 countries.

Andrea Kh StavoeDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, United States.ORCID 0000-0002-4073-4565
Pallavi P GopalDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, United States.
Andrea GubasMolecular Cell Biology of Autophagy Laboratory, The Francis Crick Institute, London, United Kingdom.
Sharon A ToozeMolecular Cell Biology of Autophagy Laboratory, The Francis Crick Institute, London, United Kingdom.
Erika Lf HolzbaurDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, United States.ORCID 0000-0001-5389-4114
University of Pennsylvania · USThe Francis Crick Institute · GB

Funding

Mechanistic analysis of axonal transport defects in neurodegenerative diseaseR37NS060698 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HOLZBAUR, ERIKA L · 2014 to 2020
$2.9M
TDP43 mRNA complex transport in physiologic and pathologic statesK08NS094744 · NINDS · YALE UNIVERSITY · PI GOPAL, PALLAVI P. · 2015 to 2019
$917k
Autophagy in aging and neurodegenerationK99NS109286 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI STAVOE, ANDREA · 2018 to 2019
$162k
Dynamic regulation of autophagy in neurons during synaptic plasticity and agingF32NS100348 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI STAVOE, ANDREA · 2017 to 2018
$118k
Cancer Research UK 15153Cancer Research UK FC001187Medical Research Council FC001187NIH HHS F32 NS100348-01NIH HHS K99 NS109286-01NIH HHS R37 NS060698NINDS NIH HHS F32 NS100348NINDS NIH HHS K08 NS094744NINDS NIH HHS K99 NS109286NINDS NIH HHS R37 NS060698Wellcome Trust FC001187
6 · The paper itself

Abstract

Autophagy defects are implicated in multiple late-onset neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS) and Alzheimer's, Huntington's, and Parkinson's diseases. Since aging is the most common shared risk factor in neurodegeneration, we assessed rates of autophagy in mammalian neurons during aging. We identified a significant decrease in the rate of constitutive autophagosome biogenesis during aging and observed pronounced morphological defects in autophagosomes in neurons from aged mice. While early stages of autophagosome formation were unaffected, we detected the frequent production of stalled LC3B-negative isolation membranes in neurons from aged mice. These stalled structures recruited the majority of the autophagy machinery, but failed to develop into LC3B-positive autophagosomes. Importantly, ectopically expressing WIPI2B effectively restored autophagosome biogenesis in aged neurons. This rescue is dependent on the phosphorylation state of WIPI2B at the isolation membrane, suggesting a novel therapeutic target in age-associated neurodegeneration.

Indexed as

AutophagyGene ExpressionAgingAnimalsAutophagosomesAutophagy-Related ProteinsMiceNeuronsPhosphate-Binding ProteinsAutophagy-Related ProteinsPhosphate-Binding ProteinsWipi2 protein, mouseagingautophagosome biogenesisautophagycell biologymouseneuronsneuroscienceWIPI2B

Identifiers

PMID31309927
PMCPMC6634969
OpenAlexW2958740406

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.