![]() ![]() Indicators of neuroinflammation including Iba1 positivity and IL-6 production were also reduced to normal levels. Pin1 activity and function were rescued despite the continuing presence of high levels of transgenic Aβ 42. ResultsįK506 can be safely and consistently delivered into juvenile APP/PS1 mice via time-release pellets to levels roughly seen in transplant patients, leading to the normalization of CN activity and reduction or elimination of AD pathologies including synapse loss, neuroinflammation, and cognitive impairment. Immunofluorescence, histology, molecular biology, and behavior were used to evaluate changes in AD pathology. ![]() Time release pellets were used to deliver constant FK506 dosage to APP/PS1 mice without deleterious manipulation or handling. AD prevalence was significantly reduced in solid organ recipients treated with FK506. The calcineurin (CN)-Pin1 signaling cascade can be selectively targeted with tacrolimus (FK506), a highly specific, FDA-approved CN inhibitor used safely for > 20 years in solid organ transplant recipients. Data suggests that early intervention at the first stages of mild cognitive impairment may have a greater chance for success. Novel approaches are desperately needed to help address this immense public health issue. Current treatments for Alzheimer’s disease (AD) have largely failed to yield significant therapeutic benefits. ![]()
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