Repositioning medication for cardiovascular and cerebrovascular disease to delay the onset and prevent progression of Al
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Online ISSN 1976-3786 Print ISSN 0253-6269
REVIEW
Repositioning medication for cardiovascular and cerebrovascular disease to delay the onset and prevent progression of Alzheimer’s disease Heeyoung Lee1 · EunYoung Kim2
Received: 28 June 2020 / Accepted: 31 August 2020 © The Pharmaceutical Society of Korea 2020
Abstract Alzheimer’s disease (AD) is a complex, progressive, neurodegenerative disorder. As with other common chronic diseases, multiple risk factors contribute to the onset and progression of AD. Many researchers have evaluated the epidemiologic and pathophysiological association between AD, cardiovascular diseases (CVDs), and cerebrovascular diseases (CBVDs), including commonly reported risk factors such as diabetes, hypertension, and dyslipidemia. Relevant therapies of CVDs/CBVDs for the attenuation of AD have also been empirically investigated. Considering the challenges of new drug development, in terms of cost and time, multifactorial approaches such as therapeutic repositioning of CVD/CBVD medication should be explored to delay the onset and progression of AD. Thus, in this review, we discuss our current understanding of the association between cardiovascular risk factors and AD, as revealed by clinical and non-clinical studies, as well as the therapeutic implications of CVD/CBVD medication that may attenuate AD. Furthermore, we discuss future directions by evaluating ongoing trials in the field. Keywords Alzheimer’s disease · Cardiovascular disease · Cerebrovascular disease · Pharmacotherapeutic implications · Drug repositioning
* EunYoung Kim [email protected] 1
Department of Clinical Medicinal Sciences, Konyang University, 121 Daehakro, Nonsan 32992, Republic of Korea
2
Evidence‑Based Research Laboratory, Division of Clinical Pharmacotherapy, College of Pharmacy, Chung-Ang University, Seoul 156‑756, Republic of Korea
Introduction Alzheimer’s disease (AD) is the most common type of dementia and exerts a significant burden on patients’ families and the public health system ("2020 Alzheimer’s disease facts and figures" 2020). Given the rapidly aging population, numerous factors, many of which are modifiable, aggravate major clinical features of AD such as cognitive decline (Bauer et al. 2014; Lee et al. 2019a, b; Morris et al. 2014; Norton et al. 2014). One such modifiable factor, cardiovascular disease (CVD), has been reported to share common pathophysiological and neuropathological features with AD, such as atherosclerosis and small vessel disease, which leads to neuronal damage or dysfunction (Santos et al. 2017). CVDs directly cause cerebrovascular events via insults to the cerebral vasculature. Cerebrovascular diseases (CBVDs) are also linked to AD in terms of the underlying mechanisms (Santos et al. 2017). Considering the synergistic interactions between CVDs and CBVDs that accelerate the progression of AD with a mixed pathology, and that people with dementia commonly have both CVDs and AD, pathophysiological evaluations of a wider scope are needed. In addition, more evidence
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