Affiliations: [a] Brighton and Sussex Medical School, University of Brighton, Falmer, Brighton, UK | [b] School of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, UK | [c] Cognitive Treatment and Research Unit, Sussex Partnership NHS Foundation Trust, Uckfield, East Sussex, UK | [d] Institute of Postgraduate Medicine, Brighton & Sussex Medical School, University of Brighton, Falmer, Brighton, UK
Correspondence:
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Correspondence to: Lucy Nelson, Medical Research Building, Brighton and Sussex Medical School, University of Sussex, BN1 9PX, UK. Tel.: +44 01273 877876; E-mail: l.nelson@bsms.ac.uk.
Abstract: Alzheimer's disease (AD) is by far the most common sporadic neurodegenerative disorder. Clinically it is associated with cognitive and other neuropsychological impairments, and neuropathologically it is distinguished by presence of amyloid-β plaques and neurofibrillary tangles. Hypertension has been traditionally associated with the etiology of vascular dementia, however, vascular risk factors including hypertension are increasingly being implicated in AD. Likewise, the importance of neuroinflammation in AD pathogenesis is also widely recognized. Data from animal and non-AD human studies suggest a close reciprocal relationship between hypertension and inflammatory systems. Much less is known on the potential pathological interaction between hypertension and inflammation in AD and its subsequent effects on amyloid and tau misfolding, aggregation, and propagation, events recognized as critical for the development and progression of AD. This review summarizes what is known about the mechanistic interactions between hypertension and inflammatory mediators and assesses their potential synergistic/additive role in AD genesis. Increasing our understanding of the pathological interactions between the recognized risk factors for AD is a worthwhile endeavor in a condition which currently has limited treatment options but an increasing number of potential preventative measures.
