Alzheimer’s disease (AD) is a neurodegenerative disorder marked by progressive cognitive decline and driven by complex pathological processes, including β-amyloid deposition, hyperphosphorylated tau aggregation, and neuroinflammation. β-Hydroxybutyrate (BHB), the predominant circulating ketone body, functions not only as an alternative energy substrate to mitigate neuronal energy deficits but also acts on multiple pathological targets central to AD progression. This review systematically summarizes the neuroprotective mechanisms of BHB in AD, focusing on mitochondrial dysfunction, pathological protein deposition, neuroinflammation, oxidative stress, and insulin resistance. Clinical studies indicate that BHB significantly improves cognition in APOE ε4-negative patients, yet current strategies for inducing endogenous ketosis or supplementing exogenous ketones face substantial challenges. Future research should focus on optimizing BHB administration protocols, defining the optimal therapeutic blood concentration range, and advancing BHB as a targeted metabolic intervention for AD. Collectively, this review provides a theoretical framework for understanding the multi-mechanistic synergy of BHB in AD and its clinical translation.