The lipid peroxidation products as possible markers of Alzheimer's disease in blood

Skoumalová, Alice; Ivica, J.; Santorova, Pavlina; Topinková, Eva; Wilhelm, J.

doi:10.1016/j.exger.2010.09.015

Cited by 37 publications

(35 citation statements)

References 22 publications

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“…During oxidative stress and in many pathological events, enhanced levels of TBARS have been reported 3,5 . A study performed by Altuntas et al, on patients with schizophrenia reports an increased level of lipid peroxidation evidenced by enhanced MDA content 28 .Very recently Skoumalová et al show a significant increase in the end-products of lipid peroxidation, called lipofuscin-like pigments (LFP) in the red blood cells of Alzheimer's disease (AD) patients compared to controls 29 . Since at present there are no reliable diagnostic biomarkers of AD in the blood, to measure these specific products of lipid peroxidation in the red cells of AD patients may be a reliable marker of this pathological condition.…”

Section: Membrane Lipidsmentioning

confidence: 99%

Biomarkers of Oxidative Stress in Red Blood Cells

Pandey¹,

Rizvi²

2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

154

110

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Section: Membrane Lipidsmentioning

confidence: 99%

Biomarkers of Oxidative Stress in Red Blood Cells

Pandey¹,

Rizvi²

2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

154

110

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“…Erythrocytes do not have sufficient mechanisms to repair oxidized lipids in their membranes, which leads to the accumulation of these products in the membranes as well as inside the cell during the erythrocyte's lifespan. Fluorescence spectroscopy studies revealed the significantly increased level of lipid peroxidation specific products in erythrocytes and plasma of AD dementia and MCI patients [73,74]. These altered molecules could potentially be applied as biomarkers for detection of early AD.…”

Section: Aβ-induced Morphological Changes In Erythrocytesmentioning

confidence: 99%

Search for Alzheimer's Disease Biomarkers in Blood Cells: Hypotheses-Driven Approach

et al. 2017

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Current Alzheimer's disease (AD) diagnostics is based on cognitive testing, and detecting amyloid Aβ and τ pathology by brain imaging and assays of cerebrospinal fluid. However, biomarkers identifying complex pathways contributing to pathology are lacking, especially for early AD. Preferably, such biomarkers should be more cost-effective and present in easily available diagnostic tissues, such as blood. Here, we summarize the recent findings of potential early AD molecular diagnostic biomarkers in blood platelets, lymphocytes and erythrocytes. We review molecular alterations which refer to such main hypotheses of AD pathogenesis as amyloid cascade, oxidative and mitochondrial stress, inflammation and alterations in cell cycle regulatory molecules. The major advantage of such biomarkers is the potential ability to indicate individualized therapies in AD patients. Alzheimer's disease (AD) is the most prevalent age-related dementia worldwide and one of the major unmet, increasing medical and economic problems of the modern world. As of 2015, there were an estimated 46.8 million people with dementia worldwide. This number will increase to an estimated 74.7 million in 2030 [1].Among the neuropathological hallmarks of AD are: the progressive loss of brain neurons, synaptic degeneration and the deposition of extracellular amyloid plaques and intracellular neurofibrillary tangles (NFTs) in such regions of the brain as the hippocampus, cortex and amygdala. Amyloid plaques consist mainly of 40-and 42-amino-acid Aβ peptides (Aβ40 and Aβ42). Peptides are proteolytic cleavage products of the Aβ protein precursor (APP) but with no fully elucidated biological function. NFTs are deposits of paired helical filaments composed mainly of hyperphosphorylated τ protein, a microtubule-stabilizing protein that maintains neuronal cell structure and axonal transport. Nevertheless, neither senile plaques nor NFTs are absolute hallmarks of AD dementia, because cognitively intact aged individuals may exhibit both pathological changes upon postmortem brain examination or as assessed by positron emission tomography amyloid and τ imaging agents (amyloid-PET and τ-PET) [2][3][4][5].Clinical AD manifests by aggravating dysfunction and weakening functional cognitive processes, linked to brain neuron loss that is both progressive and permanent [4], and that within several years leads to total dependence on the caregiver and eventually to death. Advances in our knowledge of AD have shown that clinical symptoms usually develop after a long preclinical pathogenic process, lasting for decades, making early AD detection in asymptomatic patients a subject of great interest [4,5]. Increasing proof demonstrates that the therapeutic methods' effectiveness is strictly contingent on the early diagnosis of AD, before the occurrence of massive neuron loss and dementia. This highlights the key importance of biochemical biomarkers for early AD diagnostics. AD diagnostics & demand for novel, improved biomarkersThe broadly accepted recommendations for AD diagnosis...

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“…13,14 AGEs increase the expression and activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in human endothelial cells, an important source of vascular oxidative stress in Type 2 diabetes. 15 Increased NADPH oxidase activity results in formation of free radicals and depletion of cellular antioxidants such as glutathione, glutathione peroxidase, superoxide dismutase and catalase.…”

Section: 10mentioning

confidence: 99%