Ann Arbor
Michigan, 48109-2002 United States
Available to mentor
Dr. Brooks received her B.S.E. in Engineering Science from the University of Michigan and then pursued graduate studies in Biomedical Engineering also at the University of Michigan. Following postdoctoral studies at the Institute of Gerontology, she joined the faculty in Physiology. In addition to her primary appointment in the Department of Molecular and Integrative Physiology, she holds a joint appointment the Department of Biomedical Engineering.
-
Ph.DUniversity of Michigan, United States, 1996
-
Center MemberCenter for Cell Plasticity and Organ Design
My research spans the organism, tissue, cellular and molecular levels and typically combines in vivo and in vitro approaches to investigate the impact of aging, exercise, disease, and changes in loading environment on structure-function relationships in skeletal muscle and tendon. A decrease with aging in muscle mass results from a loss of muscle fibers due to a loss of motor units. In addition to the muscle atrophy, unexplained muscle weakness remains when force is normalized by muscle cross-sectional area. The cellular and molecular mechanisms underlying muscle atrophy and weakness are studied in aging rodents. The mechanisms underlying differences in susceptibility to injury of muscles and tendons are also under active investigation. Exercise-induced skeletal muscle injury is initiated by the mechanical disruption of the muscle fiber ultrastructure. The initial mechanical damage initiates a cascade of events including an inflammatory response and degeneration of the damaged fibers. Understanding the tissue, cellular, and molecular adaptations responsible for the protection from injury provided by exercise training, especially the role of inflammation in initiating protective adaptations, is of particular interest.
-
Guzman SD, Abu-Mahfouz A, Davis CS, Ruiz LP, Macpherson PC, Brooks SV. 2023 Oct 7;PreprintDecoding muscle-resident Schwann cell dynamics during neuromuscular junction remodeling.
DOI:10.1101/2023.10.06.561193 PMID: 38370853 -
Paul TA, Macpherson PC, Janetzke TL, Davis CS, Jackson MJ, McArdle A, Brooks SV. Geroscience, 2023 Jun; 45 (3): 1899 - 1912.Journal ArticleOlder mice show decreased regeneration of neuromuscular junctions following lengthening contraction-induced injury.
DOI:10.1007/s11357-023-00774-w PMID: 36952126 -
Pollock N, Macpherson PC, Staunton CA, Hemmings K, Davis CS, Owen ED, Vasilaki A, Van Remmen H, Richardson A, McArdle A, Brooks SV, Jackson MJ. eNeuro, 2023 Mar; 10 (3):Journal ArticleDeletion of Sod1 in Motor Neurons Exacerbates Age-Related Changes in Axons and Neuromuscular Junctions in Mice.
DOI:10.1523/ENEURO.0086-22.2023 PMID: 36810149 -
Larouche JA, Mohiuddin M, Choi JJ, Ulintz PJ, Fraczek P, Sabin K, Pitchiaya S, Kurpiers SJ, Castor-Macias J, Liu W, Hastings RL, Brown LA, Markworth JF, De Silva K, Levi B, Merajver SD, Valdez G, Chakkalakal JV, Jang YC, Brooks SV, Aguilar CA. Elife, 2021 Jul 29; 10:Journal ArticleMurine muscle stem cell response to perturbations of the neuromuscular junction are attenuated with aging.
DOI:10.7554/eLife.66749 PMID: 34323217 -
Markworth JF, Brown LA, Lim E, Castor-Macias JA, Larouche J, Macpherson PCD, Davis C, Aguilar CA, Maddipati KR, Brooks SV. Aging Cell, 2021 Jun; 20 (6): e13393Journal ArticleMetabolipidomic profiling reveals an age-related deficiency of skeletal muscle pro-resolving mediators that contributes to maladaptive tissue remodeling.
DOI:10.1111/acel.13393 PMID: 34075679 -
Su Y, Ahn B, Macpherson PCD, Ranjit R, Claflin DR, Van Remmen H, Brooks SV. Free Radic Biol Med, 2021 Mar; 165: 299 - 311.Journal ArticleTransgenic expression of SOD1 specifically in neurons of Sod1 deficient mice prevents defects in muscle mitochondrial function and calcium handling.
DOI:10.1016/j.freeradbiomed.2021.01.047 PMID: 33561489 -
Bhaskaran S, Pollock N, C Macpherson P, Ahn B, Piekarz KM, Staunton CA, Brown JL, Qaisar R, Vasilaki A, Richardson A, McArdle A, Jackson MJ, Brooks SV, Van Remmen H. Aging Cell, 2020 Oct; 19 (10): e13225Journal ArticleNeuron-specific deletion of CuZnSOD leads to an advanced sarcopenic phenotype in older mice.
DOI:10.1111/acel.13225 PMID: 32886862 -
Markworth JF, Brown LA, Lim E, Floyd C, Larouche J, Castor-Macias JA, Sugg KB, Sarver DC, Macpherson PC, Davis C, Aguilar CA, Maddipati KR, Brooks SV. JCI Insight, 2020 Sep 17; 5 (18):Journal ArticleResolvin D1 supports skeletal myofiber regeneration via actions on myeloid and muscle stem cells.
DOI:10.1172/jci.insight.137713 PMID: 32750044