Results 161 to 170 of about 1,555,922 (344)

Orthogonal Ionic Liquid‐Based Extraction Strategy Enables Amyloid‐Specific Profiling of Aggregate Proteome

open access: yesAdvanced Science, EarlyView.
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

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

Endogenous Engineering Reprograms Extracellular Vesicles for Enhanced Therapeutic Function

open access: yesAdvanced Science, EarlyView.
This review explains how Extracellular vesicles‐producing cells can be endogenously engineered to load therapeutic proteins and nucleic acids. We summarize physiological and genetic strategies that harness native sorting pathways for selective cargo loading.
Jinghui Wang   +10 more
wiley   +1 more source

Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity

open access: yes, 2003
Although the accumulation of the neurotoxic peptide {beta} amyloid ({beta}A) in the CNS is a hallmark of Alzheimer's disease, the mechanism of {beta}A neurotoxicity remains controversial.
Abramov, A.Y.   +2 more
core  

A direct interaction between mitochondrial proteins and amyloid-β peptide and its significance for the development and treatment of Alzheimer’s disease

open access: yes, 2015
This work was supported by the Ministry of Education, Youth and Sports CZ (no. LD14009, no. SV/FVZ201201, no. SVV260062), COST CM1103, MH CZ - DRO (UHHK, 00179906), The Alzheimer’s Society, The Barcopel Foundation and the MSD Scottish Life Sciences fund ...
Gunn-Moore, Frank J   +5 more
core   +1 more source

Biolipid Film‐Fused Electrochemiluminescence for Multipurpose In Situ Bioassays

open access: yesAdvanced Science, EarlyView.
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

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

Temporal Interference Stimulation Enhances Neural Regeneration

open access: yesAdvanced Science, EarlyView.
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 Peressotti   +15 more
wiley   +1 more source

Kinsenoside Targets IDH1 to Restore Microglial Immune‐Metabolic Homeostasis for Alzheimer's Disease Therapy

open access: yesAdvanced Science, EarlyView.
Dysregulated TCA cycle contributes to Alzheimer's disease (AD) pathogenesis. Here, we show that microglial isocitrate dehydrogenase 1 (IDH1) is a critical driver. Elevated IDH1 disrupts citrate metabolism and mitochondrial function, exacerbating AD pathology.
Qianqian Li   +13 more
wiley   +1 more source

Amyloid beta: structure, biology and structure-based therapeutic development

open access: yesActa Pharmacologica Sinica, 2017
Guoqiang Chen   +7 more
semanticscholar   +1 more source

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