The calcium channel blocker Cav2.1 combined with amyloid beta monoclonal antibodies may reduce the occurrence of ARIA-E

Abstract

Alzheimer’s disease is the most common cause of dementia and one of the hardest diseases to cure in the world. It is a neurodegenerative disease that leads to cognitive decline and brain damage. The amyloid hypothesis is one of the most convincing hypotheses regarding its underlying mechanism. Before the advent of monoclonal antibodies, intervention measures were very limited. Despite several clinical trial failures, the FDA eventually approved two drugs, Lecanemab and Donanemab. However, in recent years, after the launch of amyloid-targeting monoclonal antibodies, some patients have experienced adverse reactions related to amyloid-associated imaging abnormalities (ARIA), including both cerebral edema-type and cerebral hemorrhage-type ARIA, which significantly impact the overall prognosis of patients. Nimodipine, a calcium channel blocker Cav2.1 with a dihydropyridine ring structure that selectively targets cerebral blood vessels, has shown significant pharmacological benefits. It has also demonstrated neuroprotective effects by crossing the blood–brain barrier (BBB). Robust studies of its therapeutic role in cerebrovascular diseases suggest that its potential application in the treatment of ARIA-E (edema-type of amyloid-related imaging abnormalities) in AD patients may be groundbreaking. Future research needs to assess the efficacy and safety of combining nimodipine amyloid monoclonal antibodies in alleviating the symptoms and reducing the occurrence of ARIA-E in Alzheimer’s disease patients.