with the hunter biden investigation. john: andy mccarthy has a brand-new op-ed and writes of course biden officials are interfering. why else has hunter skated? we talk to andy mccarthy new at 2:00 and whether or not the whistleblower will turn up the heat on biden s doj. sandra: welcome back as america reports heads into a second hour on this friday afternoon, it s been a heck of a week, john. john: continues to be a heck of an afternoon. john roberts in washington. also this hour, deflate-gate hits boston again. dozens of folks waking up to find the tires on their suvs slashed and ominous notes from a group calling itself the tire extinguishers. sandra: patting themselves on the back, a do-it-yourself movement. taking aim at suvs in the name of environmental justice. john: and in the next few minutes, the president will unveil his own environmental justice plan at the white house. we expect he will take aim at republicans. here is a little bit of a preview from
This article talks about neuroinflammation being a crucial aspect of Alzheimer's disease (AD). It explores various targets such as microglia, amyloid and tau, to develop more effective treatments and the importance of early intervention.
Increasing evidence has shown that gut dysbacteriosis may play a crucial role in neuroinflammation in Parkinson's disease (PD). However, the specific mechanisms that link gut microbiota to PD remain unexplored. Given the critical roles of blood-brain barrier (BBB) dysfunction and mitochondrial dysfunction in the development of PD, we aimed to evaluate the interactions among the gut microbiota, BBB, and mitochondrial resistance to oxidation and inflammation in PD. We investigated the effects of fecal microbiota transplantation (FMT) on the physiopathology of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. The aim was to explore the role of fecal microbiota from PD patients and healthy human controls in neuroinflammation, BBB components, and mitochondrial antioxidative capacity via the AMPK/SOD2 pathway. Compared to control mice, MPTP-treated mice exhibited elevated levels of Desulfovibrio, whereas mice given FMT from PD patients exhibited enriched levels of Akkerm
Senescent microglia are a distinct microglial phenotype present in aging brain that have been implicated in the progression of aging and age-related neurodegenerative diseases. However, the specific mechanisms that trigger microglial senescence are largely unknown. Quinolinic acid (QA) is a cytotoxic metabolite produced upon abnormal activation of microglia. Brain aging and age-related neurodegenerative diseases have an elevated concentration of QA. In the present study, we investigated whether QA promotes aging and aging-related phenotypes in microglia and C. elegans. Here, we demonstrate for the first time that QA, secreted by abnormal microglial stimulation, induces impaired mitophagy by inhibiting mitolysosome formation and consequently promotes the accumulation of damaged mitochondria due to reduced mitochondrial turnover in microglial cells. Defective mitophagy caused by QA drives microglial senescence and poor healthspan in C. elegans. Moreover, oxidative stress can mediate QA-i