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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Brain endothelial cell (EC) stress, including that induced by vascular amyloid β (Aβ) deposits in cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), contributes to cerebral blood flow impairment, blood brain barrier (BBB) damage, neurovascular unit dysfunction, microhemorrhages and hypoperfusion, precipitating neurodegeneration and neuroinflammation processes. Epidemiological and experimental evidence suggests that hyperhomocysteinemia (Hhcy) contributes to increasing AD risk as well as CAA pathology. However, the cellular and molecular mechanisms through which Aβ and Hhcy drive EC and BBB dysfunction, whether the molecular effects of these challenges are additive or independent, and possible therapeutic strategies, remain to be determined.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Alzheimer's disease (AD) is characterized- at both early and late stages- by neurovascular impairment. In AD, dysfunctional cerebral microvasculature is accompanied by an inflammatory response, contributing to Aβ and tau accumulation, brain cell stress and death, impaired clearance of metabolic waste, BBB permeability, and ultimately leading to neuronal demise and cognitive impairment. We previously showed that Aβ peptides induce mitochondrial dysregulation and caspase-mediated apoptosis in brain cells, including endothelial, glial, and smooth muscle cells.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Article Synopsis
- The blood-brain barrier (BBB) and cerebrovascular endothelial cells (ECs) are vital for maintaining brain health, but damage to ECs from amyloid-beta (Aβ) and cardiovascular risk factors (CVRF) can lead to serious issues like neurodegeneration and inflammation.
- Human brain microvascular ECs were exposed to Aβ, homocysteine (a CVRF), or both in order to study the effects on mitochondrial function and inflammatory responses.
- Results showed that Aβ increased mitochondrial reactive oxygen species (mtROS) and reduced mitochondrial respiration and ATP production, indicating mitochondrial damage, while glycolysis was upregulated as a compensatory mechanism.
Synthesis and Anticancer Studies of Pt(II) Complex Derived from 4-Phenylthiosemicarbazone.
Chem Biodivers
January 2025
Guangxi Science and Technology Normal University, School of food biochemical engineering, Tiebei road 966, 546199, Laibin, CHINA.
Although cisplatin is widely used as a first-line chemotherapy agent, it has significant side effects. Herein, we synthesized a Pt(II) complex (Pt1) derived from o-vanillin-4-phenylthiosemicarbazone ligand, and confirmed its crystal structure by X-ray crystallography. Complex Pt1 exhibited potent anticancer activity against various tested cancer cell lines, with particular efficacy against HepG-2 cells.
View Article and Find Full Text PDFReceptor-Interacting Protein Kinase 3-Mediated Modulation of Endothelial Cell Necroptosis and Mitochondrial Dysfunction through AMPK/Drp1 Signaling Pathway: Insights into the Pathophysiological Mechanisms of Lipopolysaccharide-Induced Acute Lung Injury.
Int J Med Sci
January 2025
Health Management Institute, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing 100853, China.
Article Synopsis
- Ripk3 is key in acute lung injury (ALI) by driving endothelial cell damage and inflammation, although the exact mechanisms are not fully understood.
- Studies using Ripk3-deficient mice revealed that removing Ripk3 improved lung tissue health, decreased inflammation, oxidative stress, and endothelial dysfunction after exposure to lipopolysaccharide (LPS).
- Ripk3 was found to inhibit the AMPK pathway and promote necroptosis in endothelial cells by affecting mitochondrial function, suggesting it could be a target for new treatments for ALI.
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