Abstract
Alzheimer’s disease (AD) is associated with the deposition of β-amyloid in the brain. AD accounts for over 50% of cases of dementia which results from disturbances in redox homeostasis. Indeed, increased intensity of protein oxidation and nitration as well as lipid peroxidation is observed in brain areas with considerable amounts of amyloid plaques and neurofibrillary tangles. However, little is known about the oxidoreductive balance of salivary glands in AD patients. Therefore, the aim of this study was to evaluate the antioxidant barrier and oxidative/nitrosative stress biomarkers in stimulated saliva and blood of AD patients. The study was participated by 25 AD patients and 25 non-demented controls without neurological diseases or cognitive impairment, matched by age and gender to the study group. The number of patients was determined based on a previous pilot study (test power = 0.9). We found a significant decrease in the activity of erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx), increased activity of catalase (CAT) and reduced concentration of plasma non-enzymatic antioxidants (uric acid, UA and reduced glutathione, GSH). In contrast, in the stimulated saliva of AD patients we observed significantly decreased activity of all antioxidant enzymes (SOD, CAT and GPx) as well as concentration of GSH compared to the control group. The content of lipid (malondialdehyde, MDA) and protein (advanced oxidation protein products, AOPP; advanced glycation end-products, AGE) oxidation products as well as biomarkers of nitrosative stress (peroxynitrite, nitrotyrosine) was significantly higher in both saliva and plasma of AD patients compared to the controls. In AD patients, we also observed a considerable decrease in stimulated saliva secretion and salivary total protein content, and an increase in salivary β-amyloid concentration. In conclusion, AD results in redox imbalance towards oxidative reactions, both at the level of the oral cavity and the entire body. General redox balance disturbances do not coincide with salivary redox balance disturbances. Reduction in stimulated saliva secretion in AD patients reflects secretory dysfunction of the parotid glands.
Highlights
Alzheimer’s disease (AD) is associated with the deposition of β-amyloid in the brain
Despite providing hydration of the patient’s oral cavity and collecting the material in autumn and winter, secretion of stimulated saliva in AD patients was reduced compared to their peers of the control group, as normal stimulated saliva secretion starts with the value of 0.7 mL/min
It should be noted that AD patients included in our experiment are treated with cholinesterase inhibitors (AChE-I) (Table 1)
Summary
Alzheimer’s disease (AD) is associated with the deposition of β-amyloid in the brain. In the stimulated saliva of AD patients we observed significantly decreased activity of all antioxidant enzymes (SOD, CAT and GPx) as well as concentration of GSH compared to the control group. It is known that the pathogenesis of this disease is more complex, and neuroinflammation and oxidative stress (OS) play a significant role in it The latter phenomenon is described as imbalance between excessive formation of oxygen (ROS) and nitrogen (RNS) free radicals and their neutralization. Disruption of this delicate oxidoreductive balance results in oxidative modification/destruction of numerous cellular components, leading to cell/organ dysfunction and development of diseases. In contrast to the results of Bermejo-Pareja et al.[3], Kim et al.[5] observed positive correlation between salivary Aβ and the stage of AD progression
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
