Alzheimer's disease (AD) is the most common age-related neurodegenerative disease worldwide. The pathogenesis of AD is related to the progressive neuronal apoptosis due to the advanced accumulation of extracellular amyloid beta (Aβ) peptide and intracellular neurofibrillary tangles (NFTs), which are caused by hyperphosphorylation of tau protein. The accumulation of Aβ and NFTs in AD is affected by diverse signaling pathways, such as Janus tyrosine kinase (JAK) and signal transducer and activator of transcription (STAT), which are involved in the JAK/STAT signaling pathway. This signaling pathway controls cell proliferation, differentiation, and survival. The JAK/STAT signaling pathway plays a critical role in the development of neurodegeneration and neuroinflammation in AD. Also, suppressor of cytokine signaling (SOCS), a negative regulator of the JAK/STAT signaling pathway, is also affected in AD. Nevertheless, the fundamental mechanism for the dysregulation of the JAK/STAT3/SOCS signaling pathway in AD is not completely explained. Henceforth, this review aims to explain and discuss the precise role of the JAK/STAT3/SOCS signaling pathway in AD and how targeting of this pathway could be effective in the management of AD.