Associated Papers
Hereditary Haemorrhagic Cerebrovascular Disease: Implications for Clinical Management.
Hou W et al.
Annals of Neurosciences, 2026
Aquaporin-4 and caveolin-1 as mediators of fibrinogen-driven cerebrovascular pathology in cerebral amyloid angiopathy.
Singh V et al.
Alzheimer's & Dementia : the Journal of the Alzheimer's Association, 2026
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
Cryo-EM studies of amyloid-β fibrils from human and murine brains carrying the Uppsala APP mutation (Δ690-695).
Zielinski M et al.
Acta Neuropathologica Communications, 2025
Aquaporin-4 and Caveolin-1 as Mediators of Fibrinogen-Driven Cerebrovascular Pathology in Cerebral Amyloid Angiopathy.
Singh V 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
Tg-SwDI transgenic mice: A suitable model for Alzheimer's disease and cerebral amyloid angiopathy basic research and preclinical studies.
Rodriguez-Lopez A et al.
Experimental Neurology, 2025
Cerebral proteome adaptations to amyloid angiopathy are prevented by carbonic anhydrase inhibitors.
Carlsen J et al.
Alzheimer's & Dementia : the Journal of the Alzheimer's Association, 2025
Genetics of intracerebral hemorrhage.
Kimball TN et al.
Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 2025
Reduction of orexin-expressing neurons and a unique sleep phenotype in the Tg-SwDI mouse model of Alzheimer's disease.
Wu Y et al.
Frontiers in Aging Neuroscience, 2025
Biological function of Aβ peptides revealed by analysis of membrane-association properties: Implications for Azheimer's disease pathogenesis.
Kim M et al.
Biochemical and Biophysical Research Communications, 2024
Cerebrospinal fluid shotgun proteomics identifies distinct proteomic patterns in cerebral amyloid angiopathy rodent models and human patients.
Vervuurt M et al.
Acta Neuropathologica Communications, 2024
Generation of induced pluripotent stem cell lines IRMBi003-A and IRMBi003-B from a healthy donor to model Alzheimer's disease.
Clua Provost C et al.
Stem Cell Research, 2023
Alzheimer's Disease; Mechanism, Mutations, and Applications of Nano-Medicine.
Maisam M et al.
Frontiers in Bioscience (landmark Edition), 2023
Clinical considerations in early-onset cerebral amyloid angiopathy.
Banerjee G et al.
Brain : a Journal of Neurology, 2023
Interaction of Proteins Involved in Neuronal Proteinopathies.
Kulichikhin KY et al.
Life (basel, Switzerland), 2023
Differential effects of familial Alzheimer's disease-causing mutations on amyloid precursor protein (APP) trafficking, proteolytic conversion, and synaptogenic activity.
Schilling S et al.
Acta Neuropathologica Communications, 2023
Exome Sequencing and Multigene Panel Testing in 1,411 Patients With Adult-Onset Neurologic Disorders.
Schuermans N et al.
Neurology. Genetics, 2023
Analysis of Non-Amyloidogenic Mutations in APP Supports Loss of Function Hypothesis of Alzheimer's Disease.
Kim M et al.
International Journal of Molecular Sciences, 2023
Hippocampal glial inflammatory markers are differentially altered in a novel mouse model of perimenopausal cerebral amyloid angiopathy.
Platholi J et al.
Frontiers in Aging Neuroscience, 2023
The emerging role of the HTRA1 protease in brain microvascular disease.
Haffner C
Frontiers in Dementia, 2023
Rare Amyloid Precursor Protein Point Mutations Recapitulate Worldwide Migration and Admixture in Healthy Individuals: Implications for the Study of Neurodegeneration.
Abondio P et al.
International Journal of Molecular Sciences, 2022
Calabria as a Genetic Isolate: A Model for the Study of Neurodegenerative Diseases.
Bruno F et al.
Biomedicines, 2022
Elevated expression of urokinase plasminogen activator in rodent models and patients with cerebral amyloid angiopathy.
Vervuurt M et al.
Neuropathology and Applied Neurobiology, 2022
Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer's model.
Reinitz F et al.
Elife, 2022
MDGA1 negatively regulates amyloid precursor protein-mediated synapse inhibition in the hippocampus.
Kim J et al.
Proceedings of the National Academy of Sciences of the United States of America, 2022
Transcriptomic Profile of Blood-Brain Barrier Remodeling in Cerebral Amyloid Angiopathy.
Situ M et al.
Frontiers in Cellular Neuroscience, 2022
Clinical characteristics and genotype-phenotype correlation analysis of familial Alzheimer's disease patients with pathogenic/likely pathogenic amyloid protein precursor mutations.
Liu Y et al.
Frontiers in Aging Neuroscience, 2022
Main features of hereditary cerebral amyloid angiopathies: A systematic review.
Biffi A
Cerebral Circulation - Cognition and Behavior, 2022
Cerebral Small Vessel Disease in Sporadic and Familial Alzheimer Disease.
Kalaria RN et al.
The American Journal of Pathology, 2021
Hereditary cerebral amyloid angiopathy mimicking CADASIL syndrome.
Psychogios K et al.
European Journal of Neurology, 2021
Dysregulated clock gene expression and abnormal diurnal regulation of hippocampal inhibitory transmission and spatial memory in amyloid precursor protein transgenic mice.
Fusilier AR et al.
Neurobiology of Disease, 2021
The Uppsala APP deletion causes early onset autosomal dominant Alzheimer's disease by altering APP processing and increasing amyloid β fibril formation.
Pagnon de la Vega M et al.
Science Translational Medicine, 2021
Genetic Insights into Alzheimer's Disease.
Latimer CS et al.
Annual Review of Pathology, 2021
"A case report: Co-occurrence of cerebral amyloid angiopathy and multiple sclerosis".
Kobylarek D et al.
Multiple Sclerosis and Related Disorders, 2020
An APP mutation family exhibiting white matter hyperintensities and cortical calcification in East China.
Yi Y et al.
Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2020
New Insights into the Molecular Bases of Familial Alzheimer's Disease.
D'Argenio V et al.
Journal of Personalized Medicine, 2020
Longitudinal Cognitive Decline in a Novel Rodent Model of Cerebral Amyloid Angiopathy Type-1.
Popescu DL et al.
International Journal of Molecular Sciences, 2020
Reduced Levels of Cerebrospinal Fluid/Plasma Aβ40 as an Early Biomarker for Cerebral Amyloid Angiopathy in RTg-DI Rats.
Zhu X et al.
International Journal of Molecular Sciences, 2020
The protective mutation A673T in amyloid precursor protein gene decreases Aβ peptides production for 14 forms of Familial Alzheimer's Disease in SH-SY5Y cells.
Guyon A et al.
Plos One, 2020
Familial L723P Mutation Can Shift the Distribution between the Alternative APP Transmembrane Domain Cleavage Cascades by Local Unfolding of the Ε-Cleavage Site Suggesting a Straightforward Mechanism of Alzheimer's Disease Pathogenesis.
Bocharov EV et al.
Acs Chemical Biology, 2019
The vexing complexity of the amyloidogenic pathway.
Castro MA et al.
Protein Science : a Publication of the Protein Society, 2019
Generation of induced pluripotent stem cells (iPSCs) IRMBi002-A from an Alzheimer's disease patient carrying a D694N mutation in the APP gene.
Auboyer L et al.
Stem Cell Research, 2019
Processing of Mutant β-Amyloid Precursor Protein and the Clinicopathological Features of Familial Alzheimer's Disease.
Bi C et al.
Aging and Disease, 2019