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Neural Plasticity
Volume 2018, Article ID 5257285, 9 pages
https://doi.org/10.1155/2018/5257285
Review Article

Proton Pump Inhibitors and Dementia: Physiopathological Mechanisms and Clinical Consequences

1Individualized Research Learner Program, Neuromuscular Research Division, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160, USA
2Neuroscience (NEUROS) Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63C–69, Bogotá 111221, Colombia
3Unidad de Farmacología, School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63C–69, Bogotá 111221, Colombia
4Medical Social Service, Hospital de San Francisco, Kra 8 No. 6A–121, Gacheta 251230, Colombia

Correspondence should be addressed to Mauricio Orlando Nava Mesa; se.lasu@mavanom

Received 14 November 2017; Accepted 14 February 2018; Published 21 March 2018

Academic Editor: Francisco Lopera

Copyright © 2018 Gloria Ortiz-Guerrero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Alzheimer’s disease (AD) is the most common type of dementia, mainly encompassing cognitive decline in subjects aged ≥65 years. Further, AD is characterized by selective synaptic and neuronal degeneration, vascular dysfunction, and two histopathological features: extracellular amyloid plaques composed of amyloid beta peptide (Aβ) and neurofibrillary tangles formed by hyperphosphorylated tau protein. Dementia and AD are chronic neurodegenerative conditions with a complex physiopathology involving both genetic and environmental factors. Recent clinical studies have shown that proton pump inhibitors (PPIs) are associated with risk of dementia, including AD. However, a recent case-control study reported decreased risk of dementia. PPIs are a widely indicated class of drugs for gastric acid-related disorders, although most older adult users are not treated for the correct indication. Although neurological side effects secondary to PPIs are rare, several preclinical reports indicate that PPIs might increase Aβ levels, interact with tau protein, and affect the neuronal microenvironment through several mechanisms. Considering the controversy between PPI use and dementia risk, as well as both cognitive and neuroprotective effects, the aim of this review is to examine the relationship between PPI use and brain effects from a neurobiological and clinical perspective.