{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T14:24:18Z","timestamp":1788531858386,"version":"build-2803163510"},"reference-count":167,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T00:00:00Z","timestamp":1788480000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Global population aging has driven a marked rise in the co-prevalence of osteoporosis and cognitive impairment, and a bidirectional epidemiological association between the two conditions is now supported by multiple meta-analyses. The shared biological mechanisms underlying this comorbidity, however, remain incompletely defined, and the two disorders continue to be managed within largely separate clinical disciplines.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aim and scope<\/jats:title>\n                    <jats:p>This review consolidates existing evidence into an integrative immunopathological framework in which inflammaging\u2014the chronic, low-grade, sterile systemic inflammatory state driven by senescent cells and their senescence-associated secretory phenotype (SASP)\u2014is examined as a shared upstream driver that concurrently reconfigures skeletal remodeling and central neuroimmune dynamics through the bone\u2013brain axis. We do not claim to identify novel molecular targets; rather, we synthesize an integrative perspective that has been treated in disciplinary silos.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key mechanistic themes<\/jats:title>\n                    <jats:p>At the molecular level, persistently elevated SASP-derived cytokines (IL-6, IL-1\u03b2, TNF-\u03b1) engage RANKL-dependent osteoclastogenesis in bone and prime microglial neuroinflammation in the central nervous system. Chronic NF-\u03baB signaling and NLRP3 inflammasome activation, amplified in preclinical models by mitochondrial DNA release via the cGAS-STING axis, sustain this dual pathological output. Within the bone\u2013brain axis, bone-derived endocrine signaling is remodeled during aging: osteocalcin (OCN) secretion declines, while osteocyte-derived sclerostin (SOST) rises and may antagonize Wnt\/\u03b2-catenin signaling in both compartments. Blood\u2013brain barrier disruption and peripheral immune-cell infiltration further amplify central neuroinflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Balanced appraisal<\/jats:title>\n                    <jats:p>We explicitly distinguish (i) conceptual hypotheses, (ii) preclinical (cellular and rodent) findings, and (iii) validated human data. Several widely cited mechanisms\u2014including OCN\u2013GPR158-mediated neuroprotection, cGAS-STING-driven neuroinflammation, and microbiome-based longevity signatures\u2014rest predominantly on murine models or single cohorts and require independent human validation. Microglial responses in the aging brain reflect a heterogeneous state space rather than a uniform pro-inflammatory conversion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Therapeutic implications<\/jats:title>\n                    <jats:p>Candidate bone\u2013brain dual-targeting interventions\u2014senolytics (dasatinib plus quercetin), NLRP3 inhibitors, cGAS-STING blockade, GLP-1 receptor agonists, and microbiota-targeted strategies\u2014are discussed with explicit reference to current evidence level, safety concerns, and translational limitations, rather than as established co-therapies. Dual-endpoint randomized trials enriched for elevated inflammaging biomarkers are needed before any of these agents can be positioned for clinical use in bone\u2013brain comorbidity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The inflammaging-centered framework advanced here provides a testable integrative pathophysiological perspective on bone\u2013brain aging comorbidity and a rationale for interdisciplinary \u201cbone\u2013brain integrated\u201d clinical evaluation in older adults, which we frame as an aspirational, hypothesis-generating model rather than an evidence-based standard of care.<\/jats:p>\n                  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