Can AD be identified through metabolic models?
Typ
Examensarbete för masterexamen
Master's Thesis
Master's Thesis
Program
MPCAS, Complex adaptive systems
Publicerad
2024
Författare
Sandstig, Gaston
Modellbyggare
Tidskriftstitel
ISSN
Volymtitel
Utgivare
Sammanfattning
The most common form of dementia is Alzheimer’s Disease (AD), a progressive neurodegenerative disorder, but so far no methods of curing or preventing it are known.
Amyloid-β proteins have been the focus of therapeutic development but clinical trials focused on reducing amyloid-β production or preventing its aggregation have
failed, leading to increased interests in other areas of AD pathology. There is evidence of impaired metabolism in those with AD, and in this project gene expression
data from the ROSMAP study was used to construct single-sample genome-scale metabolic models in an effort to see what differences can be discerned between models from those with AD and not. Although there was no observed separation between the groups when using PCA and t-SNE, the aggregate metabolic coverage between groups differed in several metabolic subsystems. The differences found had support in literature, but subsystems C5-branched dibasic acid metabolism, GPI anchor biosynthesis, heparan sulphate degradation, and lipoic acid metabolism had not been identified as differing in comparable in silico metabolic AD model studies
Beskrivning
Ämne/nyckelord
Alzheimer’s Disease , Genome-Scale Metabolic Model , Metabolic Dysfunction , RNA-se