AnalyzeDirect Trushina E, Nemutlu E, Zhang S, Christensen T, Camp J, Mesa J, Siddiqui A, Tamura Y, Sesaki H, Wengenack TM, Dzeja PP, Poduslo JF. Defects in mitochondrial dynamics and metabolomic signatures of evolving energetic stress in mouse models of familial Alzheimer’s disease. PLoS One. February 2012;7(2):e32737.
Full Text – Open Access
Publication Date
February 2012
How Analyze was Used
“Selective analysis of mitochondrial dynamics was done using analytical software (Analyze) that allows to trace each organelle from the first frame (a) through all 600 frames of the movie (stacked movie frames, b) to generate a final profile of movement (c). Resultant kymograph (c) is used to calculate velocities and identify the number of stationary and moving mitochondria.”
Keywords
Alzheimer Disease/genetics/metabolism
Amyloid/genetics
Animals
Biological Markers/metabolism
Brain/metabolism
Disease Models, Animal
Disease Progression
Hippocampus/metabolism
Humans
Metabolomics/methods
Mice
Mice, Inbred C57BL
Mice, Transgenic
Mitochondria/metabolism
Mutation
Neurons/metabolism
Presenilin-1/genetics
Time Factors
Author Affiliation(s)
Department of Molecular Pharmacology and Experimental Therapeutics and Neurology, Mayo Clinic, Rochester, MN, US. (ET, JM, AS)
Cardiovascular Diseases, Mayo Clinic, Rochester, MN, US. (EN, SZ, PPD)
Electron Microscopy Core Facility, Mayo Clinic, Rochester, MN, US. (TC)
Biomedical Imaging Resource, Mayo Clinic, Rochester, MN, US. (JC)
Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD, US. (YT, HS)
Departments of Neurology and Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, US. (TMW, JFP)
ID# 641
Tags: Alzheimer Disease/genetics/metabolism, Amyloid/genetics, Animal Disease Models, Animals, Biological Markers/metabolism, Brain/metabolism, Disease Progression, Hippocampus/metabolism, Humans, Inbred C57BL Mice, Metabolomics/methods, Mice, Mitochondria/metabolism, Mutation, Neurons/metabolism, Presenilin-1/genetics, Time Factors, Transgenic Mice