Evidence map›Paper›PMID 37488853›Full record

ReviewNeural regeneration research2024

SIRT2 as a potential new therapeutic target for Alzheimer's disease.

Noemi Sola-Sevilla, Elena Puerta

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  4. Blood-based proteomic signature of amyloidosis: identification of novel regulators of amyloid load.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  16. FermentedFoods (Basel, Switzerland) · 2024
    Article
  17. 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

2 authors at 1 institution in 3 countries.

Noemi Sola-SevillaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, University of Navarra, Navarra Institute for Health Research (IdiSNA), Pamplona, Spain.
Elena PuertaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, University of Navarra, Navarra Institute for Health Research (IdiSNA), Pamplona, Spain.
Creative Commons · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is the most common cause of dementia globally with an increasing incidence over the years, bringing a heavy burden to individuals and society due to the lack of an effective treatment. In this context, sirtuin 2, the sirtuin with the highest expression in the brain, has emerged as a potential therapeutic target for neurodegenerative diseases. This review summarizes and discusses the complex roles of sirtuin 2 in different molecular mechanisms involved in Alzheimer's disease such as amyloid and tau pathology, microtubule stability, neuroinflammation, myelin formation, autophagy, and oxidative stress. The role of sirtuin 2 in all these processes highlights its potential implication in the etiology and development of Alzheimer's disease. However, its presence in different cell types and its enormous variety of substrates leads to apparently contradictory conclusions when it comes to understanding its specific functions. Further studies in sirtuin 2 research with selective sirtuin 2 modulators targeting specific sirtuin 2 substrates are necessary to clarify its specific functions under different conditions and to validate it as a novel pharmacological target. This will contribute to the development of new treatment strategies, not only for Alzheimer's disease but also for other neurodegenerative diseases.

Indexed as

Alzheimer’s diseaseamyloidautophagymemoryneurodegenerative diseasesneuroinflammationsirtuin 2tau

Identifiers

PMID37488853
PMCPMC10479864
OpenAlexW4378217337

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.