SynthesisClinical and translational science2026
Can Environmental Enrichment Mitigate Cell Apoptosis in the Central Nervous System Under Adverse Health Conditions? A Systematic Review.
Synthesis in Clinical and translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled 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.
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.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Can Environmental Enrichment Mitigate Cell Apoptosis in the Central Nervous System Under Adverse Health Conditions? A Systematic Review.Clinical and translational science · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To summarize the available evidence in the literature regarding the effects of exposure to an enriched environment (EE) on the modulation of apoptotic markers in central tissue of rodents under unfavorable conditions. Searches were conducted in three databases: PubMed/Medline (70 articles), Scopus (65 articles), and EMBASE (128 articles), all of which were subjected to eligibility criteria. Of the 263 articles found, 95 duplicates were removed. After evaluating the title and abstract, 147 studies were excluded, leaving 21 articles, 16 of which were included in this systematic review. EE was implemented using various inanimate objects. The disruptive event/condition included social isolation, cerebral ischemia, stroke, postpartum depression, accelerated aging, ischemia/reperfusion, high altitude, Alzheimer's disease, hypobaric hypoxia, infrasound exposure, sepsis, and exposure to sevoflurane. Regarding the expression of apoptotic markers, after EE exposure, there was a reduction in the expression of p-IKKβ/IKKβ and p-P65/P65 in the hippocampus, a reduction in Bax, as well as cleaved Caspase-3, Cytochrome C, a reduction in the Bax/Bcl-2 ratio, and p53. As for anti-apoptotic markers, increased expression of Bcl-2 was observed following EE exposure. This systematic review concludes that the benefits of EE can reduce apoptosis through the modulation of both pro-apoptotic and anti-apoptotic genes. In this regard, EE has been shown to be an important neuroprotective tool in various adverse conditions, mitigating cognitive deficits by reducing apoptosis related to cellular stress.
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Registered trials
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.