Oxytocin enhances neurogenesis and synaptic plasticity to attenuate age-related cognitive decline in aged mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal interventional study.
PubMed 41215998 · doi:10.1016/j.ibneur.2025.10.008
What was done
Twelve-month-old mice received intraperitoneal oxytocin injections (0.5 mg/kg, five times weekly) or saline vehicle for 13 weeks. At 12 weeks, spatial learning and recognition memory were assessed using an object-place recognition task. Hippocampal neurogenesis was evaluated via doublecortin (DCX) immunohistochemistry, and synaptic plasticity was assessed by measuring glutamate receptor 1 (GluR1) and N-methyl-D-aspartate receptor subunit 2B (NMDAR2B) expression.
What was found
The abstract reports directional findings without exact numerical values, effect sizes, or confidence intervals. Compared with saline controls, oxytocin-treated mice demonstrated enhanced spatial learning and recognition memory in the object-place recognition task. Immunohistochemistry showed significantly increased DCX-positive cells in the hippocampus, alongside upregulated expression of GluR1 and NMDAR2B.
Why it matters
This study provides preclinical evidence that chronic peripheral oxytocin administration can stimulate hippocampal neurogenesis, upregulate key synaptic plasticity markers, and attenuate spatial memory decline in aged rodents.
Limits
The study was conducted in mice, limiting direct translation to human aging. The abstract does not report the total sample size, sex of the mice, or exact quantitative values and effect sizes. Post-cessation durability, non-spatial cognitive domains, and systemic side effects of chronic high-frequency oxytocin dosing were not characterized.