Results 81 to 90 of about 319,447 (239)

Quantification of neurodegeneration by measurement of brain-specific proteins [PDF]

open access: yes, 2003
Quantification of neurodegeneration in animal models is typically assessed by time-consuming and observer-dependent immunocytochemistry. This study aimed to investigate if newly developed ELISA techniques could provide an observer-independent, cost ...
Baker, D.   +5 more
core   +1 more source

Noninvasive Assessment of β‐Secretase Activity Through Click Chemistry‐Mediated Enrichment of Neuronal Extracellular Vesicles to Detect Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
This study presents the NEV β‐secretase activity assay, a groundbreaking method for noninvasive evaluation of β‐secretase activity in Alzheimer's disease (AD) patients, enabling the generation of individualized β‐secretase activity profiles.
Hyoyong Kim   +19 more
wiley   +1 more source

Post‐Translational Modifications in Cilia and Ciliopathies

open access: yesAdvanced Science, EarlyView.
This review synthesizes current understanding of post‐translational modifications (PTMs) in ciliary proteins and emphasizes their roles in ciliary formation, homeostasis, and signaling. This review also discusses the implication of PTM dysregulation in ciliopathies and explores therapeutic strategies targeting PTM‐modifying enzymes.
Jie Ran, Jun Zhou
wiley   +1 more source

Generation of Neural Organoids and Their Application in Disease Modeling and Regenerative Medicine

open access: yesAdvanced Science, EarlyView.
Neural organoids provide a versatile platform for neurological research. Advances in organoid technology have partially achieved human neural tissue complexity in terms of tissue structure, cell diversity, and neural signaling, offering insights into neural disorders and regenerative strategies. Technology advances from biomaterials, bio‐manufacturing,
Ruiqi Huang   +4 more
wiley   +1 more source

Transient Interdomain Interactions Modulate the Monomeric Structural Ensemble and Self‐Assembly of Huntingtin Exon 1

open access: yesAdvanced Science, EarlyView.
Polyglutamine (polyQ) tract expansion (≥ 36 amino acids) within the N‐terminal region of the Huntingtin protein (Httex1) causes Huntington's disease (HD), for which the underlying causes are not well‐understood. The authors performed computer simulations to understand the cause of HD at the molecular level.
Priyesh Mohanty   +2 more
wiley   +1 more source

Activation of Kir4.1 Channels by 2‐D08 Promotes Myelin Repair in Multiple Sclerosis

open access: yesAdvanced Science, EarlyView.
Multiple sclerosis causes myelin loss and neurological dysfunction. This study shows that 2‐D08, a small molecule targeting Kir4.1 channels, promotes OPCs differentiation via FYN tyrosine kinase phosphorylation and the FYN/MYRF pathway. It significantly improves myelin repair and motor deficits in EAE mice and marmosets, highlighting its potential as a
Mingdong Liu   +17 more
wiley   +1 more source

Disease modifying therapy for multiple system atrophy – Parkinsonian Type [PDF]

open access: yes, 2017
BACKGROUND: Multiple System Atrophy –Parkinsonian Type (MSA-P) is a rare, rapidly progressive neurodegenerative disease without any current treatment.
Dwyer, Sean Sullivan
core  

Kinsenoside‐Loaded Microneedle Accelerates Diabetic Wound Healing by Reprogramming Macrophage Metabolism via Inhibiting IRE1α/XBP1 Signaling Axis

open access: yesAdvanced Science, EarlyView.
Gut metabolite trimethylamine N‐oxide accumulates in the diabetic wound area to amplify macrophage inflammation via enhancing glycolysis activities. Kinsenoside induces macrophage repolarization from M1 to M2 phenotype through inhibiting IRE1α/XBP1 pathway, followed by HIF‐1α‐glycolysis axis repression and mitophagy‐oxidative phosphorylation axis ...
Li Lu   +13 more
wiley   +1 more source

Pleiotropic and Novel Phenotypes in The \u3cem\u3eDrosophila\u3c/em\u3e Gut Caused by Mutation of \u3cem\u3eDrop-Dead\u3c/em\u3e [PDF]

open access: yes, 2018
Normal gut function is vital for animal survival, and deviations from such function can contribute to malnutrition, inflammation, increased susceptibility to pathogens, diabetes, neurodegenerative diseases, and cancer.
Benske, Anika   +6 more
core   +1 more source

Neuronal FGF13 Inhibits Mitochondria‐Derived Damage Signals to Prevent Neuroinflammation and Neurodegeneration in a Mouse Model of Parkinson's Disease

open access: yesAdvanced Science, EarlyView.
This study elucidates a novel role of FGF13 in manipulating neuronal fate via mitochondrial transfer. FGF13 is identified as a mitochondria‐stabilizing protein by interacting with mitochondrial proteins. Under stress, the decrease of neuronal FGF13 fails to retain mitochondria within the cytoplasm, leading to the release of damaged mitochondria to ...
Nanshan Song   +15 more
wiley   +1 more source

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