Abstract
Oxidative stress (OS) is one of the factors that cause dementia conditions such as Alzheimer’s disease and vascular dementia (VaD). In the pathogenesis of VaD, OS is associated with risk factors that include increased age, hypertension, and stroke. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are a molecular source of reactive oxygen species (ROS). According to recent studies, inhibition of NOX activity can reduce cognitive impairment in animal models of VaD. In this article, we review the evidence linking cognitive impairment with NOX-dependent OS, including the vascular NOX and non-vascular NOX systems, in VaD.
Highlights
Vascular dementia (VaD) is the second most frequent type of dementia and accounts for 17% to 25% of all cases of dementia worldwide [1,2,3]
The brain has multiple sources of reactive oxygen species (ROS); it has been shown that membrane-bound nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) enzymes are the primary sources of ROS during aging, hypoperfusion, stroke and hypertension [15]
ROS produced by NADPH oxidases (NOX), which represent a major ROS-generation system, are often associated with the increased oxidative stress (OS) observed in the vascular dementia (VaD) and its risk factors [16,17]
Summary
Vascular dementia (VaD) is the second most frequent type of dementia and accounts for 17% to 25% of all cases of dementia worldwide [1,2,3]. The exact etiopathogenesis of VaD remains unknown, the evidence reported to date seems to indicate that it has multiple causes including cerebrovascular disease and coexisting vascular risk factors such as aging, hypertension, atherosclerosis, and stroke [7,8,9,10]. Studies measuring markers of OS in VaD are limited, there are data supporting a role for OS in this form of dementia, with most studies performed to date investigating markers of OS in the circulation [24] Those studies reported a reduction in plasma antioxidant levels [25], elevation of plasma lipid peroxidation [26,27], and increased DNA oxidation in the cerebrospinal fluid [28] of patients with VaD. Sci. 2017, 18, 2500 mitochondrial-induced OS is involved in hypertension-related vasculature damage [31], and that OS is responsible for the oxidation of low-density lipoproteins in atherosclerosis [32,33] and for the high levels of lipid hydroperoxides observed after ischemic stroke [16,34]
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