While animals across species typically experience suppressed consciousness and an increased arousal threshold during sleep, the responsiveness to specific sensory inputs persists. Previous studies have demonstrated that rhythmic and continuous vibration can enhance sleep in both animals and humans. However, the neural circuits underlying vibration‐induced sleep (VIS) and its potential therapeutic benefits on neuropathological processes in disease models remain unclear. Here, it is shown that intermittent vibration, such as cycles of 30 s on followed by 30 s off, is more effective in inducing sleep compared to continuous vibration. A clear evidence is further provided that allatostatin A (AstA)‐GABA signaling mediates short‐term intermittent vibration‐induced sleep (iVIS) by inhibiting octopaminergic arousal neurons through activating GABAA receptors. The existence of iVIS in mice is corroborated, implicating the GABAergic system in this process. Finally, intermittent vibration not only enhances sleep but also reduces amyloid‐β (Aβ) deposition and reverses memory defects in Alzheimer's disease models. In conclusion, the study defines a central neural circuit involved in mediating short‐term iVIS and the potential implications of vibration in treating sleep‐related brain disorders.