Because pink1-mutant flies exhibit a global shutdown of protein synthesis, we decided to measure the levels of individual proteins in adult flies through quantitative proteomics.
Familial forms of AD cause a loss of neurons associated with the accumulation of toxic amyloid β peptide (Aβ) and mitochondrial dysfunction. We found that flies over expressing a toxic form of Aβ (Aβ-Arc) exhibit altered components of mitochondrial complex I and one-carbon (1C) metabolism.
