Results 51 to 60 of about 8,460 (141)
The A673T mutation in the amyloid precursor protein reduces the production of β-amyloid protein from its β-carboxyl terminal fragment in cells [PDF]
, 2015 INTRODUCTION: The A673T mutation in the amyloid precursor protein (APP) protects against Alzheimer’s disease by reducing β-amyloid protein (Aβ) production.
Asuka Kokawa +6 more
core +1 more source
The Uppsala APP Mutation Promotes Wild‐Type Amyloid‐β Aggregation and Deposition In Vivo
Advanced Science, EarlyView.We investigated in vivo cross‐seeding of amyloid‐β (Aβ) isoforms in transgenic mice co‐expressing wild‐typeAβ and the Uppsala‐mutant Aβ variant (AβUpp), lacking six central residues. Weleveraged MALDI‐MS imaging and hyperspectral microscopy to follow spatio‐temporalAβ deposition.
Junyue Ge +14 more
wiley +1 more source
Molecules, 2018 The complex nature of Alzheimer’s disease calls for multidirectional treatment. Consequently, the search for multi-target-directed ligands may lead to potential drug candidates.
Dawid Panek +8 more
doaj +1 more source
GPCRs in CAR‐T Cell Immunotherapy: Expanding the Target Landscape and Enhancing Therapeutic Efficacy
Advanced Science, EarlyView.Chimeric antigen receptor T cell therapy faces dual challenges of target scarcity and an immunosuppressive microenvironment in solid tumors. This review highlights how G protein‐coupled receptors can serve as both novel targets to expand the therapeutic scope and functional modules to enhance CAR‐T cell efficacy.
Zhuoqun Liu +11 more
wiley +1 more source
, 2005 Considerable insight into the functional activity of proteins and enzymes can be obtained by studying the low-energy conformational distortions that the biopolymer can sustain. We carry out the characterization of these large scale structural changes for
Amadei A +16 more
core +1 more source
Biomarker-Drug and Liquid Biopsy Co-development for Disease Staging and Targeted Therapy: Cornerstones for Alzheimer's Precision Medicine and Pharmacology. [PDF]
, 2019 Systems biology studies have demonstrated that different (epi)genetic and pathophysiological alterations may be mapped onto a single tumor's clinical phenotype thereby revealing commonalities shared by cancers with divergent phenotypes.
Goetzl, Edward J +4 more
core +2 more sources
Advanced Science, EarlyView.Emerging evidence suggests that intraneuronal Aβ accumulation represents an early pathogenic event in Alzheimer's disease (AD). Using Drosophila AD model, this study shows that a nonsecreted serine protease Yip7 physically interacts with Aβ. This causes intraneuronal Aβ accumulation but surprisingly reduces the associated neurotoxicity, arguing that ...
Jingyun Su +4 more
wiley +1 more source
Protein Aggregates and Polyglutamine Tracts In Neurodegenerative Disease [PDF]
, 2018 The incidence of neurodegenerative diseases such as Alzheimer\u27s Disease, Parkinson\u27s Disease, Huntington\u27s Disease and other Polyglutamine Diseases is projected to dramatically increase throughout the developed world, and yet the pathology of ...
Mack, John
core +1 more source
Advanced Science, EarlyView.We developed a nanoparticle named OAF, which simultaneously targeted to both the brain and liver via the transferrin receptor 1 (TfR1) receptor, promoting lipoprotein receptor‐related protein 1 (LRP1) expression to enhance amyloid‐beta (Aβ) clearance. In AD mice model, OAF significantly reduced Aβ deposition and cognitive impairment, while a mitigating
Wenshuai Gong +8 more
wiley +1 more source
Making the final cut: pathogenic amyloid-β peptide generation by γ-secretase
Cell Stress, 2018 Alzheimer´s disease (AD) is a devastating neurodegenerative disease of the elderly population. Genetic evidence strongly suggests that aberrant generation and/or clearance of the neurotoxic amyloid-β peptide (Aβ) is triggering the disease.
Harald Steiner +3 more
doaj +1 more source