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Hyperhomocysteinemia (HHcy), characterized by elevated homocysteine (HCys) levels, is associated with increased risks of neurovascular diseases such as stroke or hydrocephalus. HHcy promotes oxidative stress, neuroinflammation, and endothelial dysfunction, disrupting the blood-brain barrier and accelerating neurodegeneration. These processes highlight HCys as both a biomarker and a potential therapeutic target in vascular-related neurological disorders.

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Peroxisome proliferator-activated receptor-γ (PPARγ) is a critical regulator of adipogenesis and bone metabolism, playing complex roles in osteoporosis. This study investigates the effects of taurine and homocysteine on PPARγ, focusing on their roles in osteoclastogenesis and bone health. In-silico analyses, including molecular docking and molecular dynamic simulations, revealed that both taurine and homocysteine bind competitively to the PPARγ ligand-binding domain, exhibiting distinctive antagonistic modes, including destabilization of PPARγ's key helices H3, H4/5, H11, and H12.

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  • * Analysis involved 2,431 cases and 1,265 healthy controls, revealing that individuals with the MTHFR variant had a significantly higher risk for conditions like respiratory distress, recurrent pregnancy loss, and intellectual disabilities.
  • * The MTHFR TT-genotype specifically indicated a high risk of abnormal phenotypes, emphasizing the importance of this genetic variant in neurodevelopmental and other health-related outcomes.
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Women are at a significantly higher risk of osteoporotic fractures, largely due to progressive bone demineralization and impaired bone microarchitecture. Low bone mineral density (BMD) is a common condition in women worldwide. Disrupted homocysteine (Hcy) metabolism has been linked to reduced BMD and increased risk of osteoporotic fractures.

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Homocysteine, an intermediate amino acid, is involved in methionine metabolism, which is crucial for various physiological pathways, including protein synthesis and DNA methylation. Elevated levels of homocysteine have been implicated as both a modifiable and unmodifiable risk factor in cardiovascular disease, influencing atherosclerotic disease formation and hypercoagulability. Mechanisms linking elevated homocysteine levels to vascular occlusion involve endothelial dysfunction, inflammation, and enhanced thrombotic potential.

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