Chronic sleep insufficiency is prevalent in modern society and has been associated with age-related neurodegenerative diseases. Loss of sleep accelerates the progression of neurodegeneration in animal models of neurological diseases. Here, we study whether chronic sleep curtailment leads to brain aging in wild-type animals without a genetic predisposition. To this aim, we used a wild-type mouse model to simulate the modern-day condition of restricted sleep and compared the brain (cortex) proteome of young sleep-restricted animals with different aged control groups. We reported the alteration of 149 proteins related to sleep and 1269 related to age with 96 proteins common between them. Through pathway analysis of proteins common to sleep and aging, it was discovered that the complement and coagulation cascade pathways were enriched by alterations of complement component 3 (C3), alpha-2-macroglobulin (A2M), fibrinogen alfa and beta chain (FGA and FGB). This is the first study indicating the possible role of the complement and coagulation pathways in brain aging mediated by chronic sleep restrictions (CSR) in mice.