Results 141 to 150 of about 602,933 (343)

Oral Exposure to Food‐Grade Nanoparticles Poses a Risk of Alzheimer's Disease‐Like Symptoms by Triggering Autophagy Defects in Neurons

open access: yesAdvanced Science, EarlyView.
Three food‐grade nanomaterials induce dysregulated RyR‐Ca2+ signaling through epigenetic modifications. This dysregulation impairs the autophagic clearance process, ultimately leading to abnormal Aβ deposition and increase phosphorylated tau levels.
Jiaxin Shang   +7 more
wiley   +1 more source

Nurr1 Orchestrates Claustrum Development and Functionality

open access: yesAdvanced Science, EarlyView.
Nurr1 (Nr4a2) is the master transcription factor to control claustrum morphogenesis and cell fate decision postmitotically by inhibiting intracellular G‐protein signaling. Nurr1 deficiency alters the transcriptomic profiles of subcortical claustral neurons into neocortical insular neurons, resulting in defected claustrum development, impaired axonal ...
Kuo Yan   +12 more
wiley   +1 more source

The Distribution of MAP-2 Phosphorylation in Cerebral Cortex of Long-Tailed Monkey Fetuses (Macaca fascicularis) in the Last Trimester of Gestation

open access: yesIndonesian Journal of Biotechnology, 2015
Memories are storage in cholinoceptive cells, the cells which are enriched with microtubule-associated protein 2 (MAP-2) that localized in the neuronal dendrite and the cell bodies.
Tri Wahyu Pangestiningsih   +2 more
doaj  

2-carba cyclic phosphatidic acid suppresses inflammation via regulation of microglial polarisation in the stab-wounded mouse cerebral cortex [PDF]

open access: gold, 2018
Kei Hashimoto   +6 more
openalex   +1 more source

Therapeutic Reprogramming of Glioblastoma Phenotypic States Using Multifunctional Heparin Nanoparticles

open access: yesAdvanced Science, EarlyView.
This study presents heparin‐derived nanoparticles (HP‐NPs) as a novel precision medicine platform that combines therapeutic and delivery functions. HP‐NPs target drug‐resistant glioblastoma stem cells, reprogramming them into a drug‐sensitive phenotype and significantly reducing tumor progression.
Vadim Le Joncour   +14 more
wiley   +1 more source

TRIM56 Aggravates Cerebral Ischemia‐Reperfusion Injury via Inhibiting KLF4‐Activated Ferroptosis Signaling

open access: yesAdvanced Science, EarlyView.
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang   +15 more
wiley   +1 more source

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