{"title":"A timeline of Ca2+/cAMP signalling: From basic research to potential therapeutics for dementia.","authors":"L. Bergantin","doi":"10.2174/1567205019666220415125447","DOIUrl":null,"url":null,"abstract":"BACKGROUND\nThe hypothesis that a dyshomeostasis of Ca2+ increases the incidence of dementia has been established. In fact, several discoveries have emphasized the concept that a decrease of the excess of Ca2+ could be an interesting pharmacological target to alleviate dementia symptoms. Aging along with a healthy brain can be supported by daily exercise, a self-control in caloric ingestion, and participating in intellectually challenging events. These lifestyle factors may alleviate the excess of Ca2+ resulted from a Ca2+ dyshomeostasis. Curiously, epidemiological, and clinical studies have also reported a clinical relationship among hypertension, diabetes and other inflammatory processes, and a higher risk for a decline of cognition. Considering the cumulative data from the scientific literature, including data of high evidence such as meta-analysis and systematic reviews, we can now link a Ca2+ dyshomeostasis as an upstream factor for hypertension, diabetes and other inflammatory processes, and dementia. Several reports have also indicated that increasing cAMP levels may induce neuroprotective outcomes, thus alleviating dementia symptoms.\n\n\nMETHODS\nFrom these concepts in mind, we found that the pharmacological manipulation of Ca2+/cAMP signalling could be a novel plausible target to treat dementia. This article puts together fundamental concepts, and current therapies, to treat dementia, including novel therapeutics coming from the pharmacological manipulation of Ca2+/cAMP signalling.\n\n\nRESULTS\nThen, combined with improvements in the lifestyle issues, these novel therapeutics may allow sustained improvements in the life quality of age-related neurological patients.\n\n\nCONCLUSIONS\nIn addition, considering coronavirus disease 2019 (COVID-19) is a rapidly evolving field, this article also reviewed recent reports about the role of Ca2+ channel blockers for restoring Ca2+ signalling disruption due to COVID-19. Finally, this article also presents a timeline of the major events in Ca2+/cAMP signaling.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Alzheimer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1567205019666220415125447","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
BACKGROUND
The hypothesis that a dyshomeostasis of Ca2+ increases the incidence of dementia has been established. In fact, several discoveries have emphasized the concept that a decrease of the excess of Ca2+ could be an interesting pharmacological target to alleviate dementia symptoms. Aging along with a healthy brain can be supported by daily exercise, a self-control in caloric ingestion, and participating in intellectually challenging events. These lifestyle factors may alleviate the excess of Ca2+ resulted from a Ca2+ dyshomeostasis. Curiously, epidemiological, and clinical studies have also reported a clinical relationship among hypertension, diabetes and other inflammatory processes, and a higher risk for a decline of cognition. Considering the cumulative data from the scientific literature, including data of high evidence such as meta-analysis and systematic reviews, we can now link a Ca2+ dyshomeostasis as an upstream factor for hypertension, diabetes and other inflammatory processes, and dementia. Several reports have also indicated that increasing cAMP levels may induce neuroprotective outcomes, thus alleviating dementia symptoms.
METHODS
From these concepts in mind, we found that the pharmacological manipulation of Ca2+/cAMP signalling could be a novel plausible target to treat dementia. This article puts together fundamental concepts, and current therapies, to treat dementia, including novel therapeutics coming from the pharmacological manipulation of Ca2+/cAMP signalling.
RESULTS
Then, combined with improvements in the lifestyle issues, these novel therapeutics may allow sustained improvements in the life quality of age-related neurological patients.
CONCLUSIONS
In addition, considering coronavirus disease 2019 (COVID-19) is a rapidly evolving field, this article also reviewed recent reports about the role of Ca2+ channel blockers for restoring Ca2+ signalling disruption due to COVID-19. Finally, this article also presents a timeline of the major events in Ca2+/cAMP signaling.
期刊介绍：
Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.
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