Articlenpj aging2026
Osteocalcin is a compensatory hormone to protect the nervous system in ovariectomized mice.
Article in npj aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
10 authors.
Funding
Abstract
Undercarboxylated osteocalcin (ucOCN), a bone-derived hormone, modulates neurocognition and emotional regulation. Its concentration declines with aging but rises secondarily in females with estrogen deficiency caused by ovarian decline. Using an ovariectomized (OVX) mouse model, we found serum ucOCN sharply increased in early OVX stages with normal behavioral performance, whereas prolonged estrogen loss decreased ucOCN and induced cognitive and emotional impairments. Ocn knockout mice failed to exhibit OVX-triggered ucOCN elevation and displayed severe synaptic damage and behavioral deficits at the early stage, which were rescued by exogenous ucOCN supplementation. Furthermore, long-term ucOCN administration ameliorated behavioral impairments induced by sustained estrogen deficiency, upregulated the expression of synaptic proteins, and restored hippocampal synaptic plasticity. Collectively, dynamic alterations in ucOCN are correlated with neurobehavioral changes under estrogen deficiency. As a time-dependent neurocompensatory mediator, ucOCN maintains hippocampal synaptic integrity. Long-term ucOCN intervention may provide a promising therapeutic strategy for estrogen deficiency-related cognitive and emotional disorders.
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