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Since brain changes often precede behavioral symptoms, identifying early markers of vulnerability is critical. Here, we investigated whether dopamine regulation and synaptic or inflammatory signaling might provide early indicators of cognitive decline, prior to behavioral impairment.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Method and Finding<\/jats:bold>\n                    : Female hooded\u2010Lister rats at 6 (young) and 12 (age\u2010unimpaired) months of age were tested using the novel object recognition (NOR) task, with no observable cognitive deficits found in either group. Biochemical analyses revealed marked molecular differences in the prefrontal cortex (PFC) of aged\u2010unimpaired rats. Synaptic proteins BDNF, PSD\u201095, and synaptophysin were significantly reduced, indicating synaptic destabilization. Concurrently, expression of COMT and NET, key regulators of dopamine catabolism and reuptake, was increased, suggesting reduced dopaminergic tone. Inflammatory signaling also shifted:\n                    <jats:italic>Nfkb<\/jats:italic>\n                    and\n                    <jats:italic>Socs3<\/jats:italic>\n                    were increased at the transcriptional level in the PFC, while\n                    <jats:italic>Il\u20106<\/jats:italic>\n                    and\n                    <jats:italic>Cox2<\/jats:italic>\n                    remained stable. In contrast, the hippocampus showed relative resistance to these changes, with no significant alterations in most markers, although NF\u2010\u03baB activation was detected at the mRNA level, indicating posttranscriptional regulation.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion<\/jats:bold>\n                    : Our findings suggest that the PFC undergoes a latent vulnerability phase during midlife, marked by synaptic and dopaminergic dysregulation alongside low\u2010grade inflammation, despite preserved cognitive performance. The hippocampus appears more resilient at this stage. Together, these early molecular changes may indicate later cognitive decline and offer a critical window for preventive intervention. Targeting these early shifts in the aging brain could hold transformative potential for delaying cognitive impairment.\n                  <\/jats:p>","DOI":"10.1002\/brb3.71395","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T05:45:29Z","timestamp":1776231929000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["The Role of Dopamine Signaling and Neuroinflammation in Age\u2010Related Cognitive Dysfunction"],"prefix":"10.1002","volume":"16","author":[{"given":"Junior","family":"Bowen","sequence":"first","affiliation":[{"name":"School of Pharmacy, Optometry and Medical Sciences University of Bradford  Bradford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katie","family":"Hanna","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Optometry and Medical Sciences University of Bradford  Bradford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew M. 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