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J Math Biol ; 82(5): 39, 2021 03 25.
Artigo em Inglês | MEDLINE | ID: mdl-33768404

RESUMO

The misconformation and aggregation of the protein Amyloid-Beta (A[Formula: see text]) is a key event in the propagation of Alzheimer's Disease (AD). Different types of assemblies are identified, with long fibrils and plaques deposing during the late stages of AD. In the earlier stages, the disease spread is driven by the formation and the spatial propagation of small amorphous assemblies called oligomers. We propose a model dedicated to studying those early stages, in the vicinity of a few neurons and after a polymer seed has been formed. We build a reaction-diffusion model, with a Becker-Döring-like system that includes fragmentation and size-dependent diffusion. We hereby establish the theoretical framework necessary for the proper use of this model, by proving the existence of solutions using a fixed point method.


Assuntos
Doença de Alzheimer , Modelos Biológicos , Doença de Alzheimer/patologia , Peptídeos beta-Amiloides , Humanos , Neurônios , Placa Amiloide
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