Results 201 to 210 of about 86,930,709 (262)

Microglial Deubiquitinase OTUD7B Stabilizes STAT3 to Promote Neuroinflammation and Cognitive Decline in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
. ABSTRACT Neuroinflammation driven by microglial activation is a defining feature of Alzheimer's disease (AD), yet the molecular mechanisms sustaining this proinflammatory state remain unclear. Here, we identify the deubiquitinase OTUD7B as a critical regulator of microglial activation and AD pathology.
Luyao Li   +15 more
wiley   +1 more source

Gm26550 Modulates Learning and Memory by Increasing IGF1 mRNA Expression and Stability in Nrf2−/− Mice

open access: yesAdvanced Science, EarlyView.
The present study shows that Nrf2 directly binds to the Gm26550 promoter, thereby activating Gm26550 transcription and increasing its expression. Mechanistically, Gm26550 promotes IGF1 expression by functionally antagonizing miR‐26a‐5p‐mediated repression and sequestering the RBP KHSRP, thereby enhancing hippocampal neuronal synaptic plasticity and ...
Hongfang Wang   +12 more
wiley   +1 more source

Smart Nanotechnologies for Multimodal Neuromodulation and Brain Interfacing

open access: yesAdvanced Science, EarlyView.
Recent advances in smart nanotechnologies are expanding the toolbox for brain interfacing, from wireless neuromodulation and high‐resolution sensing to targeted delivery within the central nervous system. By combining responsive nanomaterials with bioinspired design, these platforms enable multimodal interactions with neurons and glia, while also ...
Tommaso Curiale   +6 more
wiley   +1 more source

Ferroelectric Devices for In‐Memory and In‐Sensor Computing

open access: yesAdvanced Science, EarlyView.
Inspired by biological systems, in‐memory and in‐sensor computing overcome von Neumann bottlenecks. Ferroelectric devices can mimic synaptic functions and sense stimuli like light or force, therefore are ideal for these paradigms. This review introduces the ferroelectric devices applied for in‐memory and in‐sensor computing, covering their structures ...
Hong Fang   +5 more
wiley   +1 more source

Early Retinal UCHL1 Dysregulation Coupled With Synaptic Loss Reflects Alzheimer's Disease Severity

open access: yesAdvanced Science, EarlyView.
This study identifies synapse‐enriched deubiquitinase UCHL1 as an early Aβ‐responsive regulator of retinal synaptopathy in Alzheimer's disease. Retinal UCHL1 loss accompanies excitatory synapse degeneration, p75NTR activation, and neuroinflammation, and predicts Braak stage and cognitive decline. Aβ42 fibrils trigger synaptic and UCHL1 depletion before
Altan Rentsendorj   +25 more
wiley   +1 more source

Home - About - Disclaimer - Privacy