Abstract Alzheimer’s disease (AD) is a common neurodegenerative disorder for which effective treatments are still lacking. Recent studies have revealed that putrescine, as a central molecule in polyamine metabolism, plays a critical role in the onset and progression of AD. This review systematically summarizes the neurobiological functions of putrescine and its multifaceted pathological mechanisms in AD, including the promotion of Aβ deposition, induction of oxidative stress and mitochondrial damage, activation of neuroinflammation, and impairment of synaptic function. Additionally, the article evaluated therapeutic strategies targeting putrescine metabolism, such as inhibiting its key synthetic enzymes or supplementing beneficial polyamines, in terms of their potential and challenges in intervening with the AD process. This study provides a theoretical basis for a deeper understanding of the metabolic mechanisms of AD and the development of therapeutic approaches targeting the polyamine system.