Abstract: Alzheimer’s disease (AD), the most common type of dementia, affects millions of people worldwide, putting a significant strain on healthcare infrastructure and societal resources. AD is characterized by the build-up of amyloid-beta (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau protein. These pathological features cause neuroinflammation, vascular dysfunction, and ultimately, neuronal death and cognitive decline (Long and Holtzman, 2019). Two critical signaling pathways, the mitogen-activated protein kinase (MAPK) family and cyclin-dependent kinase 5 (CDK5), have been implicated in the pathogenesis of AD. There are three primary subfamilies within the MAPK family, namely extracellular signal-regulated kinases, c-Jun N-terminal kinases, and p38 MAPKs. Of these, p38α MAPK is particularly involved in neuroinflammation and vascular dysfunction, processes that are integral to the progression of AD. CDK5, a serine/threonine kinase primarily expressed in the central nervous system, has crucial roles in neuronal migration, synapse formation, and synaptic plasticity. However, aberrant activation of CDK5 has been linked to various neurodegenerative diseases, including AD.