Up-regulation of cholesterol synthesis pathways and limited neurodegeneration in a knock-in Sod1 mutant mouse model of ALS.
Janice A DominovLaura A MadiganJoshua P WhittKaterina L RademacherKristin M WebsterHesheng ZhangHaruhiko BannoSiqi TangYifan ZhangNicholas WightmanEmma M ShychuckJohn PageAlexandra WeissKaren KellyAlper KucukuralMichael H BrodskyAlexander JaworskiJustin R FallonDiane LipscombeRobert H BrownPublished in: bioRxiv : the preprint server for biology (2023)
mice with a severe phenotype. Our data implicate dysregulation of cholesterol or other related lipid genes in ALS pathogenesis and provide new insights that could contribute to strategies for disease intervention.
Keyphrases
- amyotrophic lateral sclerosis
- mouse model
- low density lipoprotein
- randomized controlled trial
- wild type
- electronic health record
- high fat diet induced
- genome wide
- early onset
- big data
- fatty acid
- insulin resistance
- drug induced
- gene expression
- deep learning
- adipose tissue
- skeletal muscle
- metabolic syndrome
- genome wide identification
- genome wide analysis
- data analysis