CDK5 and Alzheimer disease: The hypothesis gains further support from data obtained in NPC animal models, revealing that targeting CDK5 has the capacity to impede disease progression.51 Additionally, insights from models of ischemic stroke and Alzheimer’s disease indicate that the targeting of KV2 channel clustering is effective in slowing down the progression of disease pathology.52,53 This collective evidence underscores the potential therapeutic significance of modulating CDK5 and/or KV2.1–CaV1.2 interactions in addressing the cellular manifestations of neurodegeneration.