Evidence map›Paper›PMID 37123415›Full record

ReviewFrontiers in cell and developmental biology2023

The proteasome: A key modulator of nervous system function, brain aging, and neurodegenerative disease.

Kanisa Davidson, Andrew M Pickering

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Human iPSC models revealResearch square · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. International journal of molecular sciences · 2026
    Article
  8. Observational
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. The Ubiquitin-Proteasome System in Brain Disorders: Pathogenic Pathways, Post-Translational Tweaks, and Therapeutic Frontiers.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  20. Review
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.

Kanisa DavidsonDepartment of Psychology, University of Alabama at Birmingham, Birmingham, AL, United States.
Andrew M PickeringCenter for Neurodegeneration and Experimental Therapeutics (CNET), Department of Neurology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.
University of Alabama at Birmingham · US

Funding

Biological and environmental factors driving behavioral symptoms in Alzheimer's diseaseR01MH121928 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI PICKERING, ANDREW MICHAEL, PICKERING, CAROLYN E ZIMINSKI · 2019 to 2024
$2.9M
Proteasome dysfunction as a driver of age-associated risk for Alzheimer's disease onset and progressionRF1AG065301 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI PICKERING, ANDREW MICHAEL · 2020 to 2020
$2.1M
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 R56 AG061051NIA NIH HHS RF1 AG065301NIMH NIH HHS R01 MH121928
6 · The paper itself

Abstract

The proteasome is a large multi-subunit protease responsible for the degradation and removal of oxidized, misfolded, and polyubiquitinated proteins. The proteasome plays critical roles in nervous system processes. This includes maintenance of cellular homeostasis in neurons. It also includes roles in long-term potentiation via modulation of CREB signaling. The proteasome also possesses roles in promoting dendritic spine growth driven by proteasome localization to the dendritic spines in an NMDA/CaMKIIα dependent manner. Proteasome inhibition experiments in varied organisms has been shown to impact memory, consolidation, recollection and extinction. The proteasome has been further shown to impact circadian rhythm through modulation of a range of 'clock' genes, and glial function. Proteasome function is impaired as a consequence both of aging and neurodegenerative diseases. Many studies have demonstrated an impairment in 26S proteasome function in the brain and other tissues as a consequence of age, driven by a disassembly of 26S proteasome in favor of 20S proteasome. Some studies also show proteasome augmentation to correct age-related deficits. In amyotrophic lateral sclerosis Alzheimer's, Parkinson's and Huntington's disease proteasome function is impaired through distinct mechanisms with impacts on disease susceptibility and progression. Age and neurodegenerative-related deficits in the function of the constitutive proteasome are often also accompanied by an increase in an alternative form of proteasome called the immunoproteasome. This article discusses the critical role of the proteasome in the nervous system. We then describe how proteasome dysfunction contributes to brain aging and neurodegenerative disease.

Indexed as

Alzheimer’s diseasebrain aginghuntington’s diseaseimmunoproteasomeParkinson's diseaseproteasomesynaptic plasticityubiquitin proteasomal system

Identifiers

PMID37123415
PMCPMC10133520
OpenAlexW4365455553

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.