Evidence map›Paper›PMID 26425387›Full record

ReviewAging and disease2015

SUMOylation: Novel Neuroprotective Approach for Alzheimer's Disease?

Juliana B Hoppe, Christianne G Salbego, Helena Cimarosti

Open access · goldAbstract readReview
In one paragraph

Review in Aging and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Ubiquitin-proteasome system in the different stages of dominantly inherited Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Deciphering the SUMO code in the kidney.Journal of cellular and molecular medicine · 2019
    Review
  12. Article
  13. Article
  14. Epigenetic regulation of astrocyte function in neuroinflammation and neurodegeneration.Biochimica et biophysica acta. Molecular basis of disease · 2018
    Review
  15. Minimotifs dysfunction is pervasive in neurodegenerative disorders.Alzheimer's & dementia (New York, N. Y.) · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. The Roles of SUMO in Metabolic Regulation.Advances in experimental medicine and biology · 2017
    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

3 authors at 1 institution in 1 country.

Juliana B Hoppe1 Laboratory of Neuroprotection and Cell Signaling, Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.
Christianne G Salbego1 Laboratory of Neuroprotection and Cell Signaling, Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003, Brazil.
Helena Cimarosti2 Reading School of Pharmacy, University of Reading, Reading, RG6 6UB, UK.
Universidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized in the brain by the formation of amyloid-beta (Aβ)-containing plaques and neurofibrillary tangles containing the microtubule-associated protein tau. Neuroinflammation is another feature of AD and astrocytes are receiving increasing attention as key contributors. Although some progress has been made, the molecular mechanisms underlying the pathophysiology of AD remain unclear. Interestingly, some of the main proteins involved in AD, including amyloid precursor protein (APP) and tau, have recently been shown to be SUMOylated. The post-translational modification by SUMO (small ubiquitin-like modifier) has been shown to regulate APP and tau and may modulate other proteins implicated in AD. Here we present an overview of recent studies suggesting that protein SUMOylation might be involved in the underlying pathogenic mechanisms of AD and discuss how this could be exploited for therapeutic intervention.

Indexed as

Alzheimer’s diseaseneuroinflammationpost-translational protein modificationSUMOSUMOylation

Identifiers

PMID26425387
PMCPMC4567215
OpenAlexW1956441082

What OpenQuestion holds

Textmetadata
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.