Journal
CURRENT ALZHEIMER RESEARCH
Volume 17, Issue 4, Pages 344-354Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1567205017666200528162046
Keywords
Alzheimer's disease; calcium hypothesis; nSOCE; therapeutic agents; cytosolic space; endoplasmic reticulum (ER)
Categories
Funding
- Russian Science Foundation [18-74-00027]
- National Institutes of Health [R01 AG055577]
- state grant (IB) (chapter: TRPC6 as a molecular target) [17.991.2017/4.6]
- Russian Science Foundation [18-74-00027] Funding Source: Russian Science Foundation
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Despite decades of research and effort, there is still no effective disease-modifying treatment for Alzheimer's Disease (AD). Most of the recent AD clinical trials were targeting amyloid pathway, but all these trials failed. Although amyloid pathology is a hallmark and defining feature of AD, targeting the amyloid pathway has been very challenging due to low efficacy and serious side effects. Alternative approaches or mechanisms for our understanding of the major cause of memory loss in AD need to be considered as potential therapeutic targets. Increasing studies suggest that Ca2+ dysregulation in AD plays an important role in AD pathology and is associated with other AD abnormalities, such as excessive inflammation, increased ROS, impaired autophagy, neurodegeneration, synapse, and cognitive dysfunction. Ca2+ dysregulation in cytosolic space, Endoplasmic Reticulum (ER) and mitochondria have been reported in the context of various AD models. Drugs or strategies, to correct the Ca2+ dysregulation in AD, have been demonstrated to be promising as an approach for the treatment of AD in preclinical models. This review will discuss the mechanisms of Ca2+ dysregulation in AD and associated pathology and discuss potential approaches or strategies to develop novel drugs for the treatment of AD by targeting Ca2+ dysregulation.
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