In the brain, Oxidative Stress (OS) contribute to structural and functional changes associated with vascular aging, such as endothelial dysfunction, extracellular matrix degradation, resulting in age-related reduced vasodilatation in response to agonists. For this reason, OS is considered a key factor in Alzheimer's Disease (AD) development and recent evidence correlated oxidative stress with vascular lesion in the pathogenesis of AD, but the mechanism still need to be fully clarified. The etiology of AD is still not completely understood and is influenced by several factors including Apolipoprotein E (ApoE) genotype. In particular, the Apo ε4 isoform is considered a risk factor for AD development. This study was aimed to evaluate the possible relationship between three plasmatic OS marker and Apo ε4 carrier status. Plasmatic soluble receptor for advanced glycation end products (sRAGE) levels, plasma antioxidant total defenses (by lag-time method) and plasmatic Reactive Oxygen species (ROS) levels were evaluated in 25 AD patients and in 30 matched controls. ROS were significantly higher while plasma antioxidant total defenses and sRAGE levels were significantly lower in AD patients compared to controls. In AD patients lag-time values show a significant positive linear correlation with sRAGE levels and a (even not significant) negative correlation with ROS levels. Lag-time is significantly lower in ε4 carrier ( = 13) than in ε4 non-carrier ( = 12). Our result confirms the substantial OS in AD. Lag-time levels showed a significant positive correlation with sRAGE levels and a significant association with ε4 carrier status suggesting that plasmatic lag-time evaluation can be considered as a potential useful OS risk marker in AD.
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http://dx.doi.org/10.1186/s12979-019-0147-x | DOI Listing |
Adv Sci (Weinh)
January 2025
School of Pharmacy, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
β-secretase (BACE1) is instrumental in amyloid-β (Aβ) production, with overexpression noted in Alzheimer's disease (AD) neuropathology. The interaction of Aβ with the receptor for advanced glycation endproducts (RAGE) facilitates cerebral uptake of Aβ and exacerbates its neurotoxicity and neuroinflammation, further augmenting BACE1 expression. Given the limitations of previous BACE1 inhibition efforts, the study explores reducing BACE1 expression to mitigate AD pathology.
View Article and Find Full Text PDFLipids Health Dis
December 2024
Department of Neurology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Background: Although dyslipidemia has been acknowledged as a risk factor for Alzheimer's disease (AD), the effects of lipid-lowering drugs on AD have not been determined. The primary pathophysiological hallmark of AD is the deposition of amyloid-β (Aβ) plaques in the brain. Plasma Aβ levels are influenced by the transport of Aβ from the central nervous system to the peripheral blood.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Medical Biochemistry, Faculty of Pharmacy, Medical University of Plovdiv, 15A Vasil Aprilov Blvd., 4002 Plovdiv, Bulgaria.
J Periodontol
December 2024
Department of Oral and Maxillofacial Diseases, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Background: Advanced glycation end products (AGE) and their receptors (RAGE) have been implicated in developing periodontal complications in diabetic patients. This study aimed to identify salivary AGE, RAGE, soluble RAGE (sRAGE), and active-matrix metalloproteinase-8 (aMMP-8) levels at varying glycemic levels in periodontitis patients.
Methods: Ninety-eight participants were categorized into uncontrolled DM-PD group (n = 27)-periodontitis patients with uncontrolled Type 2 diabetes mellitus (T2DM) (glycated hemoglobin [HbA1c] ≥7%); controlled DM-PD group (n = 33)-periodontitis patients with controlled T2DM (HbA1c 5.
PLoS One
November 2024
Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
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