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
Noradrenergic innervation across brain regions is altered by aging and by disease progression in a mouse model of Alzheimer's disease neuropathology.
Hernandez NM et al.
Plos One, 2026
Effect of the Icelandic Mutation APPA673T in the Murine APP Gene on Phenotype of Line 66 Tau Mice.
Anschuetz A et al.
Biomolecules, 2025
Discovery of small molecules and a druggable groove that regulate DNA binding and release of the AP-1 transcription factor ΔFOSB.
McNeme S et al.
The Journal of Biological Chemistry, 2025
Phenotypic variability in early-onset dementia segregating with a novel APP (p.I718M) variant.
Johansson C et al.
Alzheimer's Research & Therapy, 2025
PINK1-dependent NFKB signaling contributes to amyloid pathology in Alzheimer disease.
Du F et al.
Autophagy, 2025
Meningeal vascular Aβ deposition associates with cerebral hypoperfusion and compensatory collateral remodeling.
Kaloss AM et al.
Alzheimer's Research & Therapy, 2025
Comparison of the ApoE allelic variants in the formation of intracerebral Aβ deposits.
Xu G et al.
Neurobiology of Disease, 2025
Amyloid precursor protein and C99 are subunits in human microglial Hv1 channels that enhance current and inflammatory mediator release.
Zhao R et al.
Proceedings of the National Academy of Sciences of the United States of America, 2025
Discovery of Small Molecules and a Druggable Groove That Regulate DNA Binding and Release of the AP1 Transcription Factor ΔFOSB.
McNeme S et al.
Biorxiv : the Preprint Server for Biology, 2025
Efficient in vivo pharmacological inhibition of ΔFOSB, an AP1 transcription factor, in brain.
McNeme S et al.
Biorxiv : the Preprint Server for Biology, 2025
Cytokine-induced reprogramming of human macrophages toward Alzheimer's disease-relevant molecular and cellular phenotypes in vitro.
Podleśny-Drabiniok A et al.
Cell Reports, 2025
The landscape of autosomal-dominant Alzheimer's disease: global distribution and age of onset.
Liu H et al.
Brain : a Journal of Neurology, 2025
Meningeal vascular Aβ deposition associates with cerebral hypoperfusion and compensatory collateral remodeling.
Kaloss AM et al.
Biorxiv : the Preprint Server for Biology, 2025
Impairment of Tricarboxylic Acid Cycle (TCA) Cycle in Alzheimer's Disease: Mechanisms, Implications, and Potential Therapies.
Mohan GS et al.
Aging and Disease, 2025
A single fibril study reveals that ApoE inhibits the elongation of Aβ42 fibrils in an isoform-dependent manner.
Dasadhikari S et al.
Communications Chemistry, 2025
Spectrum of γ-Secretase dysfunction as a unifying predictor of ADAD age at onset across PSEN1, PSEN2 and APP causal genes.
Fernández SG et al.
Molecular Neurodegeneration, 2025
Clinical Significance of Early-Onset Alzheimer's Mutations in Asian and Western Populations: A Scoping Review.
Poniah P et al.
Genes, 2025
The Spectrum of Genetic Risk in Alzheimer Disease.
Karagas N et al.
Neurology. Genetics, 2025
Regulatory Mechanisms and Therapeutic Implications of Lysosomal Dysfunction in Alzheimer's Disease.
Kim Y et al.
International Journal of Biological Sciences, 2025
Targeted autophagic clearance of Tau protects against Alzheimer's disease through amelioration of Tau-mediated lysosomal stress.
Yoon BH et al.
Theranostics, 2025
AAVrh.10 delivery of novel APOE2-Christchurch variant suppresses amyloid and Tau pathology in Alzheimer's disease mice.
Günaydin C et al.
Molecular Therapy : the Journal of the American Society of Gene Therapy, 2024
GNG5 is a novel regulator of Aβ42 production in Alzheimer's disease.
Li C et al.
Cell Death & Disease, 2024
Thy1-ApoE4/C/EBPβ double transgenic mice act as a sporadic model with Alzheimer's disease.
Qian Z et al.
Molecular Psychiatry, 2024
AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer's disease.
Kim YS et al.
Journal of Neuroinflammation, 2024
Frequency of Variants in Mendelian Alzheimer's Disease Genes within the Alzheimer's Disease Sequencing Project (ADSP).
Wang D et al.
Medrxiv : the Preprint Server for Health Sciences, 2024
Cryo-EM structures of cotton wool plaques' amyloid β and of tau filaments in dominantly inherited Alzheimer disease.
Hoq MR et al.
Acta Neuropathologica, 2024
Rodent Models of Alzheimer's Disease: Past Misconceptions and Future Prospects.
Collins HM et al.
International Journal of Molecular Sciences, 2024
Cryo-EM structures of amyloid-β and tau filaments in Down syndrome.
Fernandez A et al.
Nature Structural & Molecular Biology, 2024
The six brain-specific TAU isoforms and their role in Alzheimer's disease and related neurodegenerative dementia syndromes.
Buchholz S et al.
Alzheimer's & Dementia : the Journal of the Alzheimer's Association, 2024
AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer's disease.
Kim YS et al.
Biorxiv : the Preprint Server for Biology, 2024
A bidirectional link between sulfatide and Alzheimer's disease.
Zimmer VC et al.
Cell Chemical Biology, 2024
Neurodegenerative Disease Tauopathies.
Creekmore BC et al.
Annual Review of Pathology, 2024
Alzheimer's Disease: Models and Molecular Mechanisms Informing Disease and Treatments.
Nystuen KL et al.
Bioengineering (basel, Switzerland), 2024
Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease.
Srinivasan S et al.
Frontiers in Immunology, 2024
Cerebrovascular Dysfunction in Alzheimer's Disease and Transgenic Rodent Models.
Fang X et al.
Journal of Experimental Neurology, 2024
Clinical considerations in early-onset cerebral amyloid angiopathy.
Banerjee G et al.
Brain : a Journal of Neurology, 2023
Nedd4-1 regulates human sodium-dependent vitamin C transporter-2 functional expression in neuronal and epithelial cells.
Teafatiller T et al.
The Journal of Nutritional Biochemistry, 2023
Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer's Disease.
Wu YH et al.
Antioxidants (basel, Switzerland), 2023
Interaction of Proteins Involved in Neuronal Proteinopathies.
Kulichikhin KY et al.
Life (basel, Switzerland), 2023
APP family member dimeric complexes are formed predominantly in synaptic compartments.
Schilling S et al.
Cell & Bioscience, 2023
MicroRNA-128 suppresses tau phosphorylation and reduces amyloid-beta accumulation by inhibiting the expression of GSK3β, APPBP2, and mTOR in Alzheimer's disease.
Li S et al.
Cns Neuroscience & Therapeutics, 2023
Differential and substrate-specific inhibition of γ-secretase by the C-terminal region of ApoE2, ApoE3, and ApoE4.
Hou X et al.
Neuron, 2023
Endogenous recapitulation of Alzheimer's disease neuropathology through human 3D direct neuronal reprogramming.
Sun Z et al.
Biorxiv : the Preprint Server for Biology, 2023
Moesin is an effector of tau-induced actin overstabilization, cell cycle activation, and neurotoxicity in Alzheimer's disease.
Beckmann A et al.
Iscience, 2023
Apolipoprotein E4 inhibits γ-secretase activity via binding to the γ-secretase complex.
Sun Y et al.
Journal of Neurochemistry, 2023
Cryo-EM structures of amyloid-β filaments with the Arctic mutation (E22G) from human and mouse brains.
Yang Y et al.
Acta Neuropathologica, 2023
Deficiency of IKKβ in neurons ameliorates Alzheimer's disease pathology in APP- and tau-transgenic mice.
Schnöder L et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2023
Cathepsin B Deficiency Improves Memory Deficits and Reduces Amyloid-β in hAβPP Mouse Models Representing the Major Sporadic Alzheimer's Disease Condition.
Hook G et al.
Journal of Alzheimer's Disease : Jad, 2023