Results 221 to 230 of about 647,233 (310)
An orthogonal ionic‐liquid extraction (Orth‐iEA) enables selective isolation of amyloid fibrils. TMGBF4 disrupts hydrogen‐bonded β‐sheet networks to solubilize amyloid aggregates, whereas C12ImCl interacts with hydrophobic regions of non‐amyloid proteins.
Shiying Zheng +10 more
wiley +1 more source
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
Biolipid Film‐Fused Electrochemiluminescence for Multipurpose In Situ Bioassays
An ECL‐emissive, membrane‐interactive scaffold was fabricated, and facilely fused with natural and non‐native phospholipids into multifactorial mimicries of cytomembranes and vesicles for in vitro representative membrane‐process probing. Such a biointerface‐based, state‐sensitive ECL paradigm not only pinpointed proximal phenomena, including channeling
Jialiang Chen +9 more
wiley +1 more source
Smart Nanotechnologies for Multimodal Neuromodulation and Brain Interfacing
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
Temporal Interference Stimulation Enhances Neural Regeneration
Temporal interference (TI) stimulation is proposed as a non‐invasive approach to enhance neural regeneration in the deep brain. Theta‐band TI modulation selectively promotes neural progenitor cell differentiation in vitro and augments hippocampal neurogenesis in amouse model of Alzheimer's disease‐like amyloidosis.
Sofia Peressott +15 more
wiley +1 more source
SETD1A is a key epigenetic regulator in NPCs during IDD. In normal NPCs, it sustains H3K4me3–HELZ2/PPARα–HIF1α signaling to maintain glycolytic energy metabolism and proliferation. In degenerated NPCs, reduced SETD1A disrupts this axis, impairing glycolysis and accelerating senescence, highlighting a promising therapeutic target for IDD.
Jiawei Fu +11 more
wiley +1 more source

