Results 151 to 160 of about 89,643 (298)

Adaptive Network Stabilization Despite Profound Structural Reorganization in Human Organotypic Cultures

open access: yesAdvanced Science, EarlyView.
Adult human organotypic cortical slices undergo marked neuronal loss, laminar disruption, and glial activation, yet their network activity progressively stabilizes after a variable period. Electrophysiology, longitudinal calcium imaging, and quantitative histology show that structurally remodeled human circuits show adaptive capacity resulting in ...
Estilla Zsófia Tóth   +20 more
wiley   +1 more source

Neuron‐Derived Vesicular circMagi1 Restrains Vascular Repair After Ischemic Stroke by Promoting TRIM65‐Mediated ANXA2 Degradation

open access: yesAdvanced Science, EarlyView.
After ischemic stroke, injured neurons transfer circMagi1 to endothelial cells through extracellular vesicles. Within endothelial cells, circMagi1 binds ANXA2 and enhances its engagement with TRIM65, promoting ANXA2 ubiquitination and proteasomal degradation to constrain angiogenic repair.
Youkun Bi   +16 more
wiley   +1 more source

Hederagenin Attenuates Morphine Addiction via GABAA1‐Mediated Modulation of Ca2+–CaMK–CREB Signaling in Ventral Tegmental Dopaminergic Neurons

open access: yesAdvanced Science, EarlyView.
Hederagenin is identified as a GABAA1‐targeting natural compound that suppresses morphine‐associated reward by restraining Ca2+–CaMK–cAMP–CREB signaling in ventral tegmental dopaminergic neurons. RVG29‐modified liposomal delivery further enhances brain accumulation and behavioral efficacy, providing a mechanistically defined strategy for natural ...
Hongyang Jiang   +15 more
wiley   +1 more source

Temporal Trajectories of the Tau Aggregate Interactome Reveal Stage‐Specific Vulnerabilities in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
Tau populations with different aggregation states associate with distinct sets of proteins in the Alzheimer's disease brain. Proteomic discovery combined with single‐molecule analysis in neurons reveals dynamic associations involving proteostasis, metabolism and RNA biology.
Dorothea Böken   +8 more
wiley   +1 more source

A Gut‐Brain Axis Underlying Succinate‐Associated Compulsive‐Like Behavior

open access: yesAdvanced Science, EarlyView.
Gut‐derived succinate is associated with an excitatory‐inhibitory imbalance in dmPFC glutamatergic neurons, involving microglial SUCNR1 activation and vagal afferent signaling via upregulated gut 5‐HT4 receptors along the DVC‐CeA‐dmPFC circuit, changes that are linked to excessive compulsive‐like behavior.
Yi Li   +12 more
wiley   +1 more source

Role of Interleukin 34 in Pulmonary Vascular Remodeling Associated With Fibrosing Interstitial Lung Disease. [PDF]

open access: yesPulm Circ
Yokokawa T   +20 more
europepmc   +1 more source

Nuclear Translocation of PFKFB3 Promotes Disuse‐Induced Muscle Atrophy via Scaffolding Nedd4‐Mediated JunB Ubiquitination

open access: yesAdvanced Science, EarlyView.
Disuse‐induced muscle atrophy is driven by a non‐metabolic, nuclear function of the enzyme PFKFB3. Acting as a scaffold, PFKFB3 facilitates Nedd4‐mediated ubiquitination and degradation of the anti‐atrophy transcription factor JunB. Inhibiting this novel PFKFB3–Nedd4–JunB signaling axis stabilizes JunB and alleviates muscle wasting, revealing a highly ...
Mengjun Ma   +12 more
wiley   +1 more source

MANF is essential for astrocyte survival in the monkey brain. [PDF]

open access: yesProtein Cell
Xing T   +18 more
europepmc   +1 more source

NUB1 Regulates Muscle Atrophy in Lung Cancer Cachexia via NF-κB Signaling Pathway. [PDF]

open access: yesAdv Sci (Weinh)
ABSTRACT Cancer‐associated cachexia (CAC) is a devastating multifactorial syndrome characterized by progressive skeletal muscle atrophy. Its mechanisms remain incompletely clarified, with limited effective therapeutic targets. NUB1, a negative regulator of ubiquitin‐like proteins mediating protein degradation, has not been fully elucidated in CAC ...
Han Y   +13 more
europepmc   +2 more sources

Co‐activation of Selective Nicotinic Acetylcholine Receptor Subtypes Is Required for Neuroprotection against Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
ABSTRACT Beta‐amyloid peptide (Aβ)‐induced suppression of hippocampal GABAergic interneuron activity drives hyperexcitability, amyloid pathology, and cognitive impairment in Alzheimer's disease (AD), suggesting that enhancing hippocampal inhibition may be protective.
Rahmi Lee   +3 more
wiley   +1 more source

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