<p>Aging is accompanied by progressive declines in metabolic and cognitive functions. Growth hormone secretagogue receptor (GHSR), a receptor for the gut hormone ghrelin, is highly expressed in neurons and plays a crucial role in metabolic regulation. We previously reported that aged global GHSR-ablated mice are lean and insulin-sensitive, and that neuronal GHSR-deleted mice (<i>Syn1‐cre;Ghsr</i>^<i>f/f</i>) completely prevent diet‐induced obesity. However,&#xa0;the role of neuronal&#xa0;GHSR in metabolic and cognitive aging has not been elucidated. The current study aims to determine the roles of neuronal GHSR in aging metabolism and cognitive dysfunction. <i>Syn1‐cre;Ghsr</i>^<i>f/f</i> mice were subjected to cold stress, glucose- and insulin-tolerance tests, behavioral tests, and tissue analysis. Aging is accompanied by glycemic dysregulation and insulin resistance; old <i>Syn1‐cre;Ghsr</i>^<i>f/f</i> mice showed improved glucose tolerance and insulin sensitivity. Aging is associated with thermogenic impairment and cognitive decline; old <i>Syn1‐cre;Ghsr</i>^<i>f/f</i> mice showed better cold resistance and retained better recognition memory. Noticeably,&#xa0;there were&#xa0;increased expression of thermogenic makers (PGC1α and UCP1) and elevated sympathetic innervation markers (tyrosine hydroxylase and synaptophysin) in brown adipose tissue of old <i>Syn1‐cre;Ghsr</i>^<i>f/f</i> mice. Lastly, old <i>Syn1‐cre;Ghsr</i>^<i>f/f</i> mice exhibited decreased pro-inflammatory cytokines and increased neural plasticity-related markers (brain-derived neurotrophic factor, synaptophysin, and tyrosine hydroxylase) in metabolic and cognitive-relevant brain regions such as hypothalamus, cortex, and hippocampus. In conclusion, neuronal inhibition of GHSR promotes a healthy aging phenotype showing improved energy metabolism and cognitive function, which is likely contributed to the improved thermogenesis and insulin sensitivity, reduced inflammation, and restored neuronal plasticity.</p>