Results 41 to 50 of about 31,379 (232)

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad   +2 more
wiley   +1 more source

Systemic Amyloidosis – Insights by Cardiovascular Magnetic Resonance [PDF]

open access: yes, 2015
Systemic amyloidosis is the exemplar infiltrative, extracellular disease. Although it is a multi-organ disorder, cardiac involvement drives prognosis. Survival is worst in the AL amyloidosis subtype. It can affect any age and any race. There is no direct
Banypersad, SM
core  

Predictive Ability of Plasma p‐tau217 for β‐Amyloid Status: A Prospective Multicenter Study

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Plasma tau phosphorylated at threonine 217 (p‐tau217) measured with fully automated platforms has shown high accuracy for Alzheimer's disease (AD) diagnosis, but real‐world multicenter data remain limited. We aimed to validate the diagnostic performance of p‐tau217 for identifying AD pathology in a real‐world multicenter cohort ...
Miquel Massons   +33 more
wiley   +1 more source

Natural history and outcome in systemic AA amyloidosis [PDF]

open access: yes, 2007
BACKGROUND:Deposition of amyloid fibrils derived from circulating acute-phase reactant serum amyloid A protein (SAA) causes systemic AA amyloidosis, a serious complication of many chronic inflammatory disorders.
Goodman, HJB   +6 more
core  

Charge‐Reversed Lipid Nanoparticles Enable Encapsulation of Pt2L4 Nanocages for In vivo Anti‐Cancer Treatment

open access: yesAdvanced Materials, EarlyView.
Charge‐reversed lipid nanoparticles (revLNPs) enable efficient encapsulation and delivery of cationic Pt2L4 nanocages. Encapsulation preserves potent anticancer activity while improving circulation, reducing vascular leakage, and promoting favorable biodistribution in vivo.
Renzo A. Knol   +16 more
wiley   +1 more source

Real-world treatment management in hereditary transthyretin amyloidosis – an experience report and proposal for therapy switch decision criteria

open access: yesNeurological Research and Practice
Background Hereditary transthyretin amyloidosis is a rapidly progressive and lethal disease. Thanks to the increasing number of disease-modifying treatments, prognosis has improved significantly.
Duc Chu Dieu   +9 more
doaj   +1 more source

Multiorgan Dysfunction and Associated Prognosis in Transthyretin Cardiac Amyloidosis

open access: yesJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Background Transthyretin cardiac amyloidosis (ATTR‐CA) is a progressive and ultimately fatal cardiomyopathy. Biomarkers reflecting multiorgan dysfunction are of increasing importance in patients with heart failure; however, their significance in ATTR‐CA ...
Adam Ioannou   +20 more
doaj   +1 more source

Dissecting the Molecular Features of Systemic Light Chain (AL) Amyloidosis: Contributions from Proteomics

open access: yesMedicina, 2021
Amyloidoses are characterized by aggregation of proteins into highly ordered amyloid fibrils, which deposit in the extracellular space of tissues, leading to organ dysfunction.
Paola Rognoni   +4 more
doaj   +1 more source

Erythropoietin in Familial Amyloidosis ATTR V30M

open access: yes, 2013
Familial amyloidosis ATTR V30M is an hereditary disorder, the most frequent type of transthyretin related amyloidosis. The main manifestation of the disease is a sensory-motor and autonomic polyneuropathy.
Costa, P.P., Beirão, I.
core   +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

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