Evidence map›Paper›PMID 31334599›Full record

ArticleAging cell2019

Neuronal-specific proteasome augmentation via Prosβ5 overexpression extends lifespan and reduces age-related cognitive decline.

Erin Munkácsy, E Sandra Chocron, Laura Quintanilla, Christi M Gendron, Scott D Pletcher, Andrew M Pickering

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. The Hallmarks of Aging: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 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 at 2 institutions in 1 country.

Erin MunkácsyThe Sam and Ann Barshop institute for Longevity and Aging Studies, UT Health San Antonio, San Antonio, Texas.
E Sandra ChocronThe Sam and Ann Barshop institute for Longevity and Aging Studies, UT Health San Antonio, San Antonio, Texas.
Laura QuintanillaThe Sam and Ann Barshop institute for Longevity and Aging Studies, UT Health San Antonio, San Antonio, Texas.
Christi M GendronDepartment of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan.
Scott D PletcherDepartment of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan.
Andrew M PickeringThe Sam and Ann Barshop institute for Longevity and Aging Studies, UT Health San Antonio, San Antonio, Texas.ORCID 0000-0001-6635-4758
The University of Texas Health Science Center at San Antonio · USUniversity of Michigan · US

Funding

TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
Modulation of aging by Sensory PerceptionR01AG030593 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PLETCHER, SCOTT · 2007 to 2025
$6.1M
Modulation of aging through mechanisms of nutrient demand and rewardR37AG051649 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCOTT PLETCHER · 2021 to 2026
$2.3M
The role of neural signaling pathways in costs of reproduction on agingR01AG063371 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PLETCHER, SCOTT, PROMISLOW, DANIEL EDWARD · 2019 to 2023
$1.9M
Modulation of aging through mechanisms of nutrient demand and rewardR01AG051649 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PLETCHER, SCOTT · 2016 to 2020
$1.6M
Dissecting the Interplay between proteasome dysfunction, proteostasis and Alzheimer's diseaseR56AG061051 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PICKERING, ANDREW MICHAEL · 2018 to 2019
$1.5M
NIA NIH HHS R01 AG030593NIA NIH HHS R01 AG063371NIA NIH HHS R37 AG051649NIA NIH HHS R56 AG061051NIA NIH HHS T32 AG021890
6 · The paper itself

Abstract

Cognitive function declines with age throughout the animal kingdom, and increasing evidence shows that disruption of the proteasome system contributes to this deterioration. The proteasome has important roles in multiple aspects of the nervous system, including synapse function and plasticity, as well as preventing cell death and senescence. Previous studies have shown neuronal proteasome depletion and inhibition can result in neurodegeneration and cognitive deficits, but it is unclear if this pathway is a driver of neurodegeneration and cognitive decline in aging. We report that overexpression of the proteasome β5 subunit enhances proteasome assembly and function. Significantly, we go on to show that neuronal-specific proteasome augmentation slows age-related declines in measures of learning, memory, and circadian rhythmicity. Surprisingly, neuronal-specific augmentation of proteasome function also produces a robust increase of lifespan in Drosophila melanogaster. Our findings appear specific to the nervous system; ubiquitous proteasome overexpression increases oxidative stress resistance but does not impact lifespan and is detrimental to some healthspan measures. These findings demonstrate a key role of the proteasome system in brain aging.

Indexed as

LongevityAgingAnimalsCognitive DysfunctionDrosophila melanogasterNeuronsProteasome Endopeptidase ComplexProteasome Endopeptidase ComplexagingDrosophilaneurodegenerationproteasome

Identifiers

PMID31334599
PMCPMC6718538
OpenAlexW2962898654

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.