Abstract

Alzheimer′s disease (AD) represents a highly common form of dementia, but can be diagnosed in the earlier stages before dementia onset. Early diagnosis is crucial for successful therapeutic intervention. The introduction of new diagnostic biomarkers for AD is aimed at detecting underlying brain pathology. These biomarkers reflect structural or biochemical changes related to AD. Examination of cerebrospinal fluid has many drawbacks; therefore, the search for sensitive and specific blood markers is ongoing. Investigation is mainly focused on upstream processes, among which oxidative stress in the brain is of particular interest. Products of oxidative stress may diffuse into the blood and evaluating them can contribute to diagnosis of AD. However, results of blood oxidative stress markers are not consistent among various studies, as documented in this review. To find a specific biochemical marker for AD, we should concentrate on specific metabolic products formed in the brain. Specific fluorescent intermediates of brain lipid peroxidation may represent such candidates as the composition of brain phospholipids is unique. They are small lipophilic molecules and can diffuse into the blood stream, where they can then be detected. We propose that these fluorescent products are potential candidates for blood biomarkers of AD.

Highlights

  • Biochemical processes related to underlying AD pathology Lipid peroxidation in AD Blood markers of lipid peroxidation in AD Protein oxidation in AD Blood markers of protein oxidation in ADNucleid acid oxidation in AD Blood markers of DNA/RNA oxidation in AD Blood antioxidants in AD Are blood markers of oxidative stress specific for AD? Specific fluorescent products of lipid peroxidation Conclusion AbstractAlzheimer′s disease (AD) represents a highly common form of dementia, but can be diagnosed in the earlier stages before dementia onset

  • Alzheimer′s disease (AD) is a progressive neurodegenerative disorder of the brain that is characterized by a loss of neurons because of extracellular accumulation of amyloid beta (Ab) and intracellular hyperphosphorylation of the tau protein

  • The results showed an increase in protein modification in AD and MCI patients compared with age-matched control individuals[63]

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Summary

Introduction

Alzheimer′s disease (AD) is a progressive neurodegenerative disorder of the brain that is characterized by a loss of neurons because of extracellular accumulation of amyloid beta (Ab) and intracellular hyperphosphorylation of the tau protein. The study was performed to evaluate the level of oxidative DNA damage in two groups of MCI and AD patients compared with healthy controls. These results are in agreement with the widespread belief that pathological processes in the brain in AD are accompanied by oxidative stress [11]. As oxidative stress accompanies other diseases, such as diabetes, cardiovascular disease and other neurodegenerative diseases, the detection of products of free radical reactions may not be specific to AD and MCI. Discriminant functions constructed using biochemical markers of oxidative stress (superoxide dismutase, catalase, glutathione, thiobarbituric acid reactive substancesand antioxidant capacity of plasma) separated patients with AD from vascular dementia, but not patients with Parkinson′s disease from AD or vascular dementia [44]

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