Synthetic Route of 19430-93-4, As an important bridge between the micro and macro material world, chemistry is one of the main methods and means for humans to understand and transform the material world. 19430-93-4, Name is 3,3,4,4,5,5,6,6,6-Nonafluorohex-1-ene, SMILES is C=CC(F)(F)C(F)(F)C(F)(F)C(F)(F)F, belongs to pyridazines compound. In a article, author is Foster, Joshua B., introduce new discover of the category.
Enhancement of tripartite synapses as a potential therapeutic strategy for Alzheimer’s disease: a preclinical study in rTg4510 mice
Background The lack of effective treatment options for Alzheimer’s disease (AD) is of momentous societal concern. Synaptic loss is the hallmark of AD that correlates best with impaired memory and occurs early in the disease process, before the onset of clinical symptoms. We have developed a small-molecule, pyridazine-based series that enhances the structure and function of both the glial processes and the synaptic boutons that form the tripartite synapse. Previously, we have shown that these pyridazine derivatives exhibit profound efficacy in an amyloid precursor protein AD model. Here, we evaluated the efficacy of an advanced compound, LDN/OSU-0215111, in rTg4510 mice-an aggressive tauopathy model. Methods rTg4510 mice were treated orally with vehicle or LDN/OSU-0215111 (10 mg/kg) daily from the early symptomatic stage (2 months old) to moderate (4 months old) and severe (8 months old) disease stages. At each time point, mice were subjected to a battery of behavioral tests to assess the activity levels and cognition. Also, tissue collections were performed on a subset of mice to analyze the tripartite synaptic changes, neurodegeneration, gliosis, and tau phosphorylation as assessed by immunohistochemistry and Western blotting. At 8 months of age, a subset of rTg4510 mice treated with compound was switched to vehicle treatment and analyzed behaviorally and biochemically 30 days after treatment cessation. Results At both the moderate and severe disease stages, compound treatment normalized cognition and behavior as well as reduced synaptic loss, neurodegeneration, tau hyperphosporylation, and neuroinflammation. Importantly, after 30 days of treatment cessation, the benefits of compound treatment were sustained, indicating disease modification. We also found that compound treatment rapidly and robustly reduced tau hyperphosphorylation/deposition possibly via the inhibition of GSK3 beta. Conclusions The results show that LDN/OSU-0215111 provides benefits for multiple aspects of tauopathy-dependent pathology found in Alzheimer’s disease including tripartite synapse normalization and reduction of toxic tau burden, which, in turn, likely accounted for normalized cognition and activity levels in compound-treated rTg4510 mice. This study, in combination with our previous work regarding the benefit of pyridazine derivatives against amyloid-dependent pathology, strongly supports pyridazine derivatives as a viable, clinically relevant, and disease-modifying treatment for many of the facets of Alzheimer’s disease.
Synthetic Route of 19430-93-4, Consequently, the presence of a catalyst will permit a system to reach equilibrium more quickly, but it has no effect on the position of the equilibrium as reflected in the value of its equilibrium constant.I hope my blog about 19430-93-4 is helpful to your research.
Reference:
Pyridazine – Wikipedia,
,Pyridazine | C4H4N2 – PubChem