Affiliations: [a] Dementia Research Group, John James Laboratories, Frenchay Hospital, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol, UK | [b] Department of Geriatrics, Center for Ageing Brain, Memory Unit, University of Bari, Bari, Italy
Correspondence:
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Correspondence to: Patrick G. Kehoe, Dementia Research Group, John James Laboratories, Frenchay Hospital, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol BS16 1LE, UK. Tel.: +44 117 340 3070; Fax: +44 117 340 6665; E-mail: [email protected].
Abstract: Midlife hypertension is a risk factor for late onset Alzheimer's disease (AD) and it is one of the components of metabolic syndrome (MetS). Observational studies and some cardiovascular disease-related clinical trials suggest that antihypertensive treatment reduced the incidence and progression of AD. Calcium channel blockers (CCBs), one of the more commonly used treatments for hypertension, target voltage-gated calcium channels (VGCCs) which are found on neurons in the brain where calcium regulation is very important in both learning and memory. Amyloid-β (Aβ) peptide, one of the main pathological hallmarks of AD, causes increases to intracellular calcium via VGCCs, which in turn leads to further increases in Aβ production. Memantine, a current treatment used in AD, exerts some of its beneficial effects by blocking calcium entry into neurons. We explore the possibility of whether CCBs acting in the brain may delay the onset and progression of AD and thus may inform treatment regimes in people with MetS.
