Search Results - "Brink, Lauren E."

  • Showing 1 - 4 results of 4
Refine Results
  1. 1

    Cuprizone-induced oligodendrocyte loss and demyelination impairs recording performance of chronically implanted neural interfaces by Wellman, Steven M., Guzman, Kelly, Stieger, Kevin C., Brink, Lauren E., Sridhar, Sadhana, Dubaniewicz, Mitchell T., Li, Lehong, Cambi, Franca, Kozai, Takashi D.Y.

    Published in Biomaterials (01-05-2020)
    “…Biological inflammation induced during penetrating cortical injury can disrupt functional neuronal and glial activity within the cortex, resulting in potential…”
    Get full text
    Journal Article
  2. 2

    Conditional depletion of GSK3b protects oligodendrocytes from apoptosis and lessens demyelination in the acute cuprizone model by Xing, Bin, Brink, Lauren E., Maers, Kelly, Sullivan, Mara L., Bodnar, Richard J., Stolz, Donna B., Cambi, Franca

    Published in Glia (01-09-2018)
    “…Apoptosis is recognized as the main mechanism of oligodendrocyte loss in Multiple Sclerosis caused either by immune mediated injury (Barnett & Prineas, ) or a…”
    Get full text
    Journal Article
  3. 3

    Conditional depletion of Fus in oligodendrocytes leads to motor hyperactivity and increased myelin deposition associated with Akt and cholesterol activation by Guzman, Kelly M., Brink, Lauren E., Rodriguez‐Bey, Guillermo, Bodnar, Richard J., Kuang, Lisha, Xing, Bin, Sullivan, Mara, Park, Hyun J., Koppes, Erik, Zhu, Haining, Padiath, Quasar, Cambi, Franca

    Published in Glia (01-10-2020)
    “…Fused in sarcoma (FUS) is a predominantly nuclear multifunctional RNA/DNA‐binding protein that regulates multiple aspects of gene expression. FUS mutations are…”
    Get full text
    Journal Article
  4. 4

    C onditional depletion of GSK 3b protects oligodendrocytes from apoptosis and lessens demyelination in the acute cuprizone model by Xing, Bin, Brink, Lauren E., Maers, Kelly, Sullivan, Mara L., Bodnar, Richard J., Stolz, Donna B., Cambi, Franca

    Published in Glia (01-09-2018)
    “…Apoptosis is recognized as the main mechanism of oligodendrocyte loss in Multiple Sclerosis caused either by immune mediated injury (Barnett & Prineas, ) or a…”
    Get full text
    Journal Article