Nature Communications (Jul 2022)

[11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer’s disease

  • Tharick A. Pascoal,
  • Mira Chamoun,
  • Elad Lax,
  • Hsiao-Ying Wey,
  • Monica Shin,
  • Kok Pin Ng,
  • Min Su Kang,
  • Sulantha Mathotaarachchi,
  • Andrea L. Benedet,
  • Joseph Therriault,
  • Firoza Z. Lussier,
  • Frederick A. Schroeder,
  • Jonathan M. DuBois,
  • Baileigh G. Hightower,
  • Tonya M. Gilbert,
  • Nicole R. Zürcher,
  • Changning Wang,
  • Robert Hopewell,
  • Mallar Chakravarty,
  • Melissa Savard,
  • Emilie Thomas,
  • Sara Mohaddes,
  • Sarah Farzin,
  • Alyssa Salaciak,
  • Stephanie Tullo,
  • A. Claudio Cuello,
  • Jean-Paul Soucy,
  • Gassan Massarweh,
  • Heungsun Hwang,
  • Eliane Kobayashi,
  • Bradley T. Hyman,
  • Bradford C. Dickerson,
  • Marie-Christine Guiot,
  • Moshe Szyf,
  • Serge Gauthier,
  • Jacob M. Hooker,
  • Pedro Rosa-Neto

DOI
https://doi.org/10.1038/s41467-022-30653-5
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 11

Abstract

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The link between amyloid and tau proteins with Alzheimer’s disease progression remains unclear. Here, the authors propose HDACs I downregulation as an element linking the deleterious effects of brain proteinopathies with disease progression.