{"title":"The calcium channel blocker Cav2.1 combined with amyloid beta monoclonal antibodies may reduce the occurrence of ARIA-E","authors":"Dinghao An , Xiaotong Li , Yun Xu","doi":"10.1016/j.mehy.2025.111576","DOIUrl":null,"url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"196 ","pages":"Article 111576"},"PeriodicalIF":2.1000,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical hypotheses","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306987725000155","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
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.
期刊介绍:
Medical Hypotheses is a forum for ideas in medicine and related biomedical sciences. It will publish interesting and important theoretical papers that foster the diversity and debate upon which the scientific process thrives. The Aims and Scope of Medical Hypotheses are no different now from what was proposed by the founder of the journal, the late Dr David Horrobin. In his introduction to the first issue of the Journal, he asks ''what sorts of papers will be published in Medical Hypotheses? and goes on to answer ''Medical Hypotheses will publish papers which describe theories, ideas which have a great deal of observational support and some hypotheses where experimental support is yet fragmentary''. (Horrobin DF, 1975 Ideas in Biomedical Science: Reasons for the foundation of Medical Hypotheses. Medical Hypotheses Volume 1, Issue 1, January-February 1975, Pages 1-2.). Medical Hypotheses was therefore launched, and still exists today, to give novel, radical new ideas and speculations in medicine open-minded consideration, opening the field to radical hypotheses which would be rejected by most conventional journals. Papers in Medical Hypotheses take a standard scientific form in terms of style, structure and referencing. The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific communication, which ideas must eventually enter if they are to be critiqued and tested against observations.