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Signs of cross-seeding: aortic medin amyloid as a trigger for protein AA deposition

Annika Larsson1, Susanna Malmström, Per Westermark

  • 1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.

Amyloid : the International Journal of Experimental and Clinical Investigation : the Official Journal of the International Society of Amyloidosis
|November 11, 2011
PubMed

Insights

Localized medin amyloidosis may initiate other amyloid diseases. This "senile" amyloidosis, common in older adults, can promote the aggregation of serum amyloid A protein, suggesting a cross-seeding mechanism for diverse amyloid deposition patterns.

Area of Science:

  • Biochemistry
  • Pathology
  • Immunology

Background:

  • Systemic amyloidoses exhibit diverse deposition patterns, often unexplained.
  • Localized medin amyloidosis (AMed), derived from lactadherin, is highly prevalent in the thoracic aorta of individuals over 50.
  • Systemic amyloidoses also deposit in the aorta, raising questions about potential interactions.

Purpose of the Study:

  • To investigate if medin amyloidosis influences the tissue distribution of serum amyloid A (AA) amyloidosis.
  • To explore the potential cross-seeding mechanism between different amyloid types.

Main Methods:

  • Analysis of seven aortas from patients with systemic AA amyloidosis using double-labeling immunofluorescence.
  • In vitro studies to assess the effect of medin amyloid fibrils on protein AA aggregation.

Main Results:

  • Partial co-localization of medin and AA aggregates was observed in four out of seven AA amyloidosis aortas.
  • In vitro experiments demonstrated that medin amyloid-like fibrils promote the aggregation of protein AA into new fibrils.

Conclusions:

  • The frequent "senile" medin amyloidosis may initiate fibril formation in less common amyloidoses.
  • A cross-seeding mechanism is proposed, explaining how prevalent amyloidoses could influence the development of others.

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