2026-06-30T03:03:56Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/182992024-11-28T14:45:59Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927
Repisalud
author
Duran-Aniotz, Claudia
author
Moreno-Gonzalez, Ines
author
Gamez, Nazaret
author
Perez-Urrutia, Nelson
author
Vegas-Gomez, Laura
author
Soto, Claudio
author
Morales, Rodrigo
authoraffiliation
[Duran-Aniotz,C; Moreno-Gonzalez,I; Gamez,N; Perez-Urrutia,N; Soto,C; Morales,R] Department of Neurology, The University of Texas Health Science Center at Houston, Fannin, St. Houston, USA. [Duran-Aniotz,C] Center for Social and Cognitive Neuroscience (CSCN), School of Psychology, Universidad Adolfo Ibanez, Santiago, Chile. [Duran-Aniotz,C] Latin American Brain Health Institute (BrainLat), Universidad Adolfo Ibanez, Santiago, Chile. [Duran-Aniotz,C; Soto,C] Universidad de los Andes, Facultad de Medicina, Las Condes, Santiago, Chile. [Moreno-Gonzalez,I; Gamez,N; Vegas-Gomez,L] Department of Cell Biology, Faculty of Sciences, University of Malaga-IBIMA, Malaga, Spain. [Moreno-Gonzalez,I] Networking Research Center On Neurodegenerative Diseases (CIBERNED), Madrid, Spain. [Moreno-Gonzalez,I; Morales,R] Centro Integrativo de Biologia Y Quimica Aplicada (CIBQA), Universidad Bernardo O’Higgins, Santiago, Chile.
2024-02-19T15:26:43Z
2024-02-19T15:26:43Z
2021-03-30
10.1186/s40478-021-01155-0
2051-5960
Acta Neuropathologica Communications
http://hdl.handle.net/10668/3905
33785065
http://hdl.handle.net/20.500.12105/18299
Amyloid-β (Aβ) misfolding is one of the hallmark pathological features of Alzheimer's disease (AD). AD can manifest with diverse symptomatology including variable rates of cognitive decline, duration of clinical disease, and other detrimental changes. Several reports suggest that conformational diversity in misfolded Aβ is a leading factor for clinical variability in AD, analogous to what it has been described for prion strains in prion diseases. Notably, prion strains generate diverse patterns of misfolded protein deposition in the brains of affected individuals. Here, we tested the in vivo prion-like transmission features of four AD brains displaying particular patterns of amyloidosis. AD brains induced different phenotypes in recipient mice, as evaluated by their specific seeding activity, as well as the total amount of Aβ deposited surrounding vascular structures and the reactivity of amyloid pathology to thioflavin S. Our results support the notion that AD-subtypes are encoded in disease-associated Aβ. Further research exploring whether AD include a spectrum of different clinical conditions or syndromes may pave the way to personalized diagnosis and treatments.
eng
Alzheimer’s disease
Amyloid-beta
Pathology
Prions
Strains
Enfermedad de alzheimer
beta-Amiloides
Patología
Priones
Amyloid pathology arrangements in Alzheimer's disease brains modulate in vivo seeding capability
research article