Dataset Information
Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease
Ontology highlight
ABSTRACT: This model is described in the article: Abstract: Despite extensive research, the pathogenesis of neurodegenerative Alzheimer's disease (AD) still eludes our comprehension. This is largely due to complex and dynamic cross-talks that occur among multiple cell types throughout the aging process. We present a mathematical model that helps define critical components of AD pathogenesis based on differential rate equations that represent the known cross-talks involving microglia, astroglia, neurons, and amyloid-? (A?). We demonstrate that the inflammatory activation of microglia serves as a key node for progressive neurodegeneration. Our analysis reveals that targeting microglia may hold potential promise in the prevention and treatment of AD. This model is hosted on BioModels Database and identified by: MODEL1409240001. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.
ORGANISM(S): Homo sapiens
SUBMITTER: Audald Lloret i Villas
PROVIDER: MODEL1409240001 | biostudies-other |
SECONDARY ACCESSION(S): 21179474
REPOSITORIES: biostudies-other
Publications
Mathematical modeling for the pathogenesis of Alzheimer's disease.
PloS one 20101214 12
Despite extensive research, the pathogenesis of neurodegenerative Alzheimer's disease (AD) still eludes our comprehension. This is largely due to complex and dynamic cross-talks that occur among multiple cell types throughout the aging process. We present a mathematical model that helps define critical components of AD pathogenesis based on differential rate equations that represent the known cross-talks involving microglia, astroglia, neurons, and amyloid-β (Aβ). We demonstrate that the inflamm ...[more]
