Associated Papers
Human in vitro and rodent in vivo models highlight progressive mitochondrial dysfunction as a starting point of cerebral amyloidosis.
Motamed Z et al.
Neurobiology of Aging, 2026
Isogenic cortical organoids enable precision targeting of APP variant-specific pathways in Alzheimer's disease.
Grass T et al.
Biorxiv : the Preprint Server for Biology, 2026
Diabetes-linked metabolic dysfunction relates with distinct tau phosphorylation patterns, neuroinflammation and cognitive impairment in mouse models of Alzheimer's disease.
Vargas-Soria M et al.
Brain, Behavior, and Immunity, 2026
Membrane-associated periodic skeleton regulates major forms of endocytosis in neurons through a signaling-driven positive feedback loop.
Fei J et al.
Biorxiv : the Preprint Server for Biology, 2026
Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Chou CC et al.
Nature Cell Biology, 2025
γ-Secretase modulator resistance of an aggressive Alzheimer-causing presenilin mutant can be overcome in the heterozygous patient state by a set of advanced compounds.
Trambauer J et al.
Alzheimer's Research & Therapy, 2025
Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Chou CC et al.
Biorxiv : the Preprint Server for Biology, 2025
The AβA2V paradigm: From molecular insights to therapeutic strategies in Alzheimer's disease and primary tauopathies.
Diomede L et al.
Pharmacological Research, 2025
A TrkB and TrkC partial agonist restores deficits in synaptic function and promotes activity-dependent synaptic and microglial transcriptomic changes in a late-stage Alzheimer's mouse model.
Latif-Hernandez A et al.
Alzheimer's & Dementia : the Journal of the Alzheimer's Association, 2024
Human tNeurons reveal aging-linked proteostasis deficits driving Alzheimer's phenotypes.
Chou CC et al.
Research Square, 2024
Simple modeling of familial Alzheimer's disease using human pluripotent stem cell-derived cerebral organoid technology.
Choe MS et al.
Stem Cell Research & Therapy, 2024
A TrkB and TrkC partial agonist restores deficits in synaptic function and promotes activity-dependent synaptic and microglial transcriptomic changes in a late-stage Alzheimer's mouse model.
Latif-Hernandez A et al.
Biorxiv : the Preprint Server for Biology, 2023
APP family member dimeric complexes are formed predominantly in synaptic compartments.
Schilling S et al.
Cell & Bioscience, 2023
DYRK1A antagonists rescue degeneration and behavioural deficits of in vivo models based on amyloid-β, Tau and DYRK1A neurotoxicity.
Zhu B et al.
Scientific Reports, 2022
Absence of tissue transglutaminase reduces amyloid-beta pathology in APP23 mice.
Wilhelmus MMM et al.
Neuropathology and Applied Neurobiology, 2022
The Transglutaminase-2 Interactome in the APP23 Mouse Model of Alzheimer's Disease.
Wilhelmus MMM et al.
Cells, 2022
The Impact of the hAPP695SW Transgene and Associated Amyloid-β Accumulation on Murine Hippocampal Biochemical Pathways.
Khorani M et al.
Journal of Alzheimer's Disease : Jad, 2022
No Association between Single Nucleotide Polymorphisms (SNPs) of the Interferon-Induced Transmembrane Protein 3 (IFITM3) Gene and the Susceptibility of Alzheimer's Disease (AD).
Won SY et al.
Medicina (kaunas, Lithuania), 2021
Tau associated peripheral and central neurodegeneration: Identification of an early imaging marker for tauopathy.
Marquez A et al.
Neurobiology of Disease, 2021
Neuronal Aquaporin 1 Inhibits Amyloidogenesis by Suppressing the Interaction Between Beta-Secretase and Amyloid Precursor Protein.
Park J et al.
The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 2021
Small molecule modulation of the p75 neurotrophin receptor inhibits multiple amyloid beta-induced tau pathologies.
Yang T et al.
Scientific Reports, 2020
Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques.
Natunen T et al.
Molecular Neurodegeneration, 2020
Retinal thinning of inner sub-layers is associated with cortical atrophy in a mouse model of Alzheimer's disease: a longitudinal multimodal in vivo study.
Chiquita S et al.
Alzheimer's Research & Therapy, 2019
Somatic APP gene recombination in Alzheimer's disease and normal neurons.
Lee MH et al.
Nature, 2018
Rab21, a Novel PS1 Interactor, Regulates γ-Secretase Activity via PS1 Subcellular Distribution.
Sun Z et al.
Molecular Neurobiology, 2018
DNA damage-associated oligodendrocyte degeneration precedes amyloid pathology and contributes to Alzheimer's disease and dementia.
Tse KH et al.
Alzheimer's & Dementia : the Journal of the Alzheimer's Association, 2018
Altered Expression of Urea Cycle Enzymes in Amyloid-β Protein Precursor Overexpressing PC12 Cells and in Sporadic Alzheimer's Disease Brain.
Jęśko H et al.
Journal of Alzheimer's Disease : Jad, 2018
Disease Progression-Dependent Effects of TREM2 Deficiency in a Mouse Model of Alzheimer's Disease.
Jay TR et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2017
ABCA1 is Necessary for Bexarotene-Mediated Clearance of Soluble Amyloid Beta from the Hippocampus of APP/PS1 Mice.
Corona AW et al.
Journal of Neuroimmune Pharmacology : the Official Journal of the Society on Neuroimmune Pharmacology, 2016
Central role for PICALM in amyloid-β blood-brain barrier transcytosis and clearance.
Zhao Z et al.
Nature Neuroscience, 2015
Novel therapeutic strategy for neurodegeneration by blocking Aβ seeding mediated aggregation in models of Alzheimer's disease.
Eleuteri S et al.
Neurobiology of Disease, 2015
LCAT deficiency does not impair amyloid metabolism in APP/PS1 mice.
Stukas S et al.
Journal of Lipid Research, 2014
Early fear memory defects are associated with altered synaptic plasticity and molecular architecture in the TgCRND8 Alzheimer's disease mouse model.
Steele JW et al.
The Journal of Comparative Neurology, 2014
Tenascin-C deficiency ameliorates Alzheimer's disease-related pathology in mice.
Xie K et al.
Neurobiology of Aging, 2013
Early BDNF treatment ameliorates cell loss in the entorhinal cortex of APP transgenic mice.
Nagahara AH et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2013
Latrepirdine (Dimebon®), a potential Alzheimer therapeutic, regulates autophagy and neuropathology in an Alzheimer mouse model.
Steele JW et al.
Autophagy, 2013
β-arrestin1 regulates γ-secretase complex assembly and modulates amyloid-β pathology.
Liu X et al.
Cell Research, 2013
A novel Rac1 GAP splice variant relays poly-Ub accumulation signals to mediate Rac1 inactivation.
Huang TY et al.
Molecular Biology of the Cell, 2013
Pericyte loss influences Alzheimer-like neurodegeneration in mice.
Sagare AP et al.
Nature Communications, 2013
Good gene, bad gene: new APP variant may be both.
Di Fede G et al.
Progress in Neurobiology, 2012
Ryanodine receptor blockade reduces amyloid-β load and memory impairments in Tg2576 mouse model of Alzheimer disease.
Oulès B et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2012
Increased Aβ production prompts the onset of glucose intolerance and insulin resistance.
Jiménez-Palomares M et al.
American Journal of Physiology. Endocrinology and Metabolism, 2012
Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer's disease.
Sheng B et al.
Journal of Neurochemistry, 2012
Similar pattern of peripheral neuropathy in mouse models of type 1 diabetes and Alzheimer's disease.
Jolivalt CG et al.
Neuroscience, 2012
Genetic animal models of cerebral vasculopathies.
Lee JH et al.
Progress in Molecular Biology and Translational Science, 2012
Alzheimer's disease-linked mutations in presenilin-1 result in a drastic loss of activity in purified γ-secretase complexes.
Cacquevel M et al.
Plos One, 2012
Amyloid protein-mediated differential DNA methylation status regulates gene expression in Alzheimer's disease model cell line.
Sung HY et al.
Biochemical and Biophysical Research Communications, 2011
Lysosomal proteolysis inhibition selectively disrupts axonal transport of degradative organelles and causes an Alzheimer's-like axonal dystrophy.
Lee S et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2011
Effect of glycogen synthase kinase 3 β-mediated presenilin 1 phosphorylation on amyloid β production is negatively regulated by insulin receptor cleavage.
Maesako M et al.
Neuroscience, 2011