UNDERSTAND THE
PATHOPHYSIOLOGY

Pathogenic TTR
is at the source of
clinical symptoms and
ATTR progression1-8

TTR SYNTHESIS
ATTR is caused by changes in TTR, a tetrameric protein primarily synthesized in the liver.
TETRAMER DISSOCIATION
TTR tetramers become less stable and dissociate into monomers and fragments.
MONOMER AGGREGATION
TTR monomers and fragments misfold and aggregate into pathogenic amyloid fibrils.
AMYLOID DEPOSITION
TTR amyloid deposits accumulate in the heart, nerves, gastrointestinal tract, and other tissues, causing damage that leads to clinical symptoms.
DISEASE PROGRESSION
Continued accumulation of amyloid deposits results in worsening clinical symptoms over time.

Learn more about the mechanism of disease behind ATTR

Early detection and intervention are critical to slow disease progression.7,9

NEXT Identifying ATTR

ATTR=transthyretin-mediated amyloidosis; TTR=transthyretin.

References:

  1. Shin SC, et al. Mt Sinai J Med. 2012;79(6):733-748.
  2. Koike H, et al. Biomedicines. 2019;7(1):11.
  3. Adams D, et al. Neurology. 2015;85(8):675-682.
  4. Adams D, et al. Curr Opin Neurol. 2016;29(suppl 1):S14-S26.
  5. Sekijima Y. J Neurol Neurosurg Psychiatry. 2015;86(9):1036-1043.
  6. Nativi-Nicolau JN, et al. Heart Fail Rev. 2022;27(3):785-793.
  7. Kittleson MM, et al. J Am Coll Cardiol. 2023;81(11):1076-1126.
  8. Hazenberg BPC. Rheum Dis Clin North Am. 2013;39(2):323-345.
  9. Kittleson MM, et al. Circulation. 2020;142(1):e7-e22.