Caloric restriction in DNA-repair-deficient mice: premature aging and cognition
In mice whose forebrain neurons lacked the DNA-repair enzyme Apex1, cognitive deficits appeared early; a 30% caloric restriction regimen from 8 to 48 weeks markedly attenuated these premature aging features and improved cognitive outcomes. [1]
Automatic summary · not editorially reviewed
The key findings
Apex1, essential for base-excision repair, was conditionally knocked out in mouse forebrain neurons. [1]
Apex1 conditional knockout mice showed spatial learning and memory deficits at 8–12 weeks and impaired long-term potentiation at 48 weeks. [1]
A 30% caloric restriction regimen from 8 to 48 weeks markedly attenuated premature aging features and improved cognitive outcomes in these mice. [1]
The source at a glance
- Study type / format
- Preclinical mouse study (abstract)
- Population / context
- Mice with conditional knockout of Apex1 in forebrain neurons
- Summary based on
- Study abstract
- Original publication
- May 8, 2026
Apex1 removal in mouse forebrain neurons
The abstract describes a conditional knockout of Apex1, an enzyme essential for base-excision repair, in forebrain neurons of mice. The stated context is that DNA damage, especially oxidative DNA damage, is a major molecular driver of senescence and aging, while Apex1's role in protecting the brain from age-related deterioration was unclear.
Supporting source [1]
Early cognitive deficits and later synaptic changes
According to the abstract, Apex1 conditional knockout mice showed early and progressive cognitive impairment, with deficits in spatial learning and memory at 8–12 weeks. At 48 weeks they also showed reduced synaptic proteins, altered neuronal morphology and impaired long-term potentiation.
Supporting source [1]
30% caloric restriction from 8 to 48 weeks
The abstract reports that a 30% caloric restriction regimen given from 8 to 48 weeks markedly attenuated these premature aging features and improved cognitive outcomes in the Apex1 conditional knockout mice. The authors present Apex1 as a critical genomic maintenance factor in the aging brain and the model as a tool for studying dietary interventions against aging.
Supporting source [1]
How to interpret this
This is an abstract; the full text was not reviewed. Findings come from a mouse model with Apex1 removed in forebrain neurons, so they do not establish effects in people or in mice with normal DNA repair. The abstract reports no sample sizes, and the cognitive and synaptic measures are described without effect sizes or statistical detail.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wei CZ, Shi Y, Zhang W, Hassan SH, Shi R, Pu H, Mu H, Anne Stetler R, Leak RK, Chen J. · europepmc.org · May 8, 2026