Brun Ulfhake, M.D., Ph.D.

Brun Ulfhake, Ph.D.

Research Focus

Impairment of the neuronal functions (senses, motor control and cognition) and the gradual loss of skeletal muscle mass and power are typical features of the aged phenotype. In muscles there is a loss of fibers and a fiber atrophy; while in the nervous system neurons are being loaded with lysosomes filled with nondegradable waste and giant mitochondria, and marked by axon atrophy, axon dystrophy, and loss of synaptic contacts. The stigmata of aging myocytes and neurons suggest impaired protein degradation; insufficient DNA repair and reduced energy production as significant components of the aging process. We address these issues by (1) investigating alterations in the activity and expression of the ubiquitin-proteasomal system and the autophagy-lysosomal system in skeletal muscle and the nervous system (NS), and how these two pathways interact. (2) We use substrate assays to investigate if alterations in base excision repair cause accumulation of DNA damage during aging and methylation assays as a first step to explore if aging associates with changes in the organization of DNA. (3) Calorie restriction, mice carrying mutations in genes encoding radical scavengers and mitochondrial repair enzyme are used as models on energy metabolism and mitochondrial impairment. We use behaviorally characterization as an instrument to assess aging-dependent impairments at the system and organismal level independent of biochemical analysis. Below please find 5 recent publications reflecting our current line of research.

Selected Publications