Evidence map›Paper›PMID 42909413›Full record

ReviewFrontiers in aging neuroscience2026

Pyroptosis: a potential target and research progress of exercise in ameliorating Alzheimer's disease pathology.

Shao Jie, Zhu Lei

Abstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Shao JieSchool of Physical Education, Qufu Normal University, Qufu, Shandong, China.
Zhu LeiSchool of Physical Education, Qufu Normal University, Qufu, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD), a debilitating neurodegenerative disorder that severely threatens elderly health, is clinically manifested as cognitive decline and driven by core pathological hallmarks including amyloid-beta (Aβ) deposition, tau hyperphosphorylation, and chronic neuroinflammation. Recent studies have indicated that its pathophysiological process is closely associated with pyroptosis, and excessive activation of pyroptosis drives a vicious cycle of amplified inflammation and neuronal injury. Although accumulating evidence suggests that exercise serves as an effective non-pharmacological intervention to suppress pyroptosis and alleviate AD, the intrinsic interactive mechanisms among exercise, pyroptosis and the pathological progression of AD remain incompletely elucidated. Therefore, this review systematically summarizes the functional mechanisms of pyroptosis in the pathological progression of AD and discusses the potential neuroprotective effects of exercise intervention. It further focuses on analyzing the specific mechanisms by which exercise inhibits pyroptosis via regulating the NLRP3 inflammasome pathway, aiming to identify novel targets for the prevention and treatment of AD and provide a theoretical basis for formulating scientific exercise intervention strategies.

Indexed as

Alzheimer’s diseaseexerciseinflammasomeneuronal injurypyroptosis

Identifiers

PMID42909413
PMCPMC13684484

What OpenQuestion holds

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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.