Results 221 to 230 of about 279,988 (315)

Microglia‐Targeted Biomimetic Tetrahedral Framework Nucleic Acid Nanovesicles for Synergistic Treatment of Sepsis‐Associated Encephalopathy

open access: yesAdvanced Science, EarlyView.
Sepsis‐associated encephalopathy (SAE) lacks effective therapies. We developed ME@FDsi, a biomimetic nanodrug using a tetrahedral framework nucleic acid to deliver disulfiram and siTNFα. It crosses the blood‐brain barrier, targets M1 microglia, inhibits pyroptosis and inflammation, and scavenges ROS.
Huimin Shi   +15 more
wiley   +1 more source

Gasdermin D‐Mediated Release of IL‐33 Results in Fetal Brain Developmental Abnormalities During Maternal Colitis

open access: yesAdvanced Science, EarlyView.
Under colitis, Gsdmd mediates the release of IL‐33 from the epithelium of pregnant mice. IL‐33 can cross the placenta and enhance the proliferative capacity of neural stem cells, ultimately resulting in behavioral deficits in the offspring. Excessive pyroptosis in the colonic epithelium also triggers the translocation of LPS, which in turn increases ...
Huiyang Jia   +4 more
wiley   +1 more source

Distinct dendritic cell cytoskeletal programs dictate synapse architecture and CD8<sup>+</sup> T cell fate. [PDF]

open access: yesFront Immunol
Clamagirand CD   +6 more
europepmc   +1 more source

Divergent Roles of mGlu2 and mGlu3 Receptors in Amyloid‐β Production and Cognitive Dysfunctions in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
This study explores the opposing effects of the mGluR2 and mGluR3 receptors on amyloid precursor protein processing. mGluR2 promotes amyloidogenic cleavage, while mGluR3 favors non‐amyloidogenic pathways. Using a brain‐penetrant nanobody as a mGluR2 positive allosteric modulator, the study uncovers how its chronic activation aggravates amyloid‐β burden
Pierre‐André Lafon   +21 more
wiley   +1 more source

Janus Synapses as Modular Neurointerfaces. [PDF]

open access: yesACS Appl Mater Interfaces
Cho W, Jung M, Chung TD.
europepmc   +1 more source

Lilrb4a Suppression Reprograms Microglia to Mitigate APOE4‐Associated Amyloid Plaques and Cerebral Amyloid Angiopathy in Association With a PPAR‐Linked Pro‐Clearance State

open access: yesAdvanced Science, EarlyView.
Targeting Lilrb4a in Apolipoprotein E4 (APOE4)‐associated Alzheimer's disease (AD) reprograms microglia toward a beneficial, phagocytic state. Genetic deletion or antisense inhibition of Lilrb4a suppresses p‐SHP2/NF‐κB/STAT1 signaling, restores PPAR‐linked lipid and energy metabolism, and reduces amyloid plaque burden and cerebral amyloid angiopathy ...
Changxu Nie   +12 more
wiley   +1 more source

AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction. [PDF]

open access: yesActa Neuropathol
Dunot J   +16 more
europepmc   +1 more source

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