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Proteoglycans and amyloid fibrillogenesis

R Kisilevsky¹, P Fraser

¹Department of Pathology, Queen's University, Kingston General Hospital, Ontario, Canada.

Ciba Foundation Symposium

|January 1, 1996

Summary

Heparan sulfate proteoglycans interact with amyloid precursors, influencing amyloid deposition. This interaction suggests new therapeutic strategies for amyloid-based diseases by targeting small molecules.

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Area of Science:

Biochemistry
Molecular Biology
Pathology

Background:

Amyloids are diverse protein aggregates implicated in various diseases.
Proteoglycans, particularly heparan sulfate proteoglycans, play roles in cellular processes.
The relationship between proteoglycans and amyloid formation in vivo is not fully understood.

Purpose of the Study:

To investigate the temporal and anatomical relationship between heparan sulfate proteoglycans and amyloid deposition.
To explore the in vitro effect of heparan sulfate on amyloid precursor structure.
To propose general concepts for interfering with amyloidogenesis.

Main Methods:

Utilized murine inflammation-associated (AA) amyloid model.
Examined in vivo temporal and anatomical correlations.
Performed in vitro studies on the effect of heparan sulfate on amyloid precursors and peptides.
Assessed the impact of small molecule aliphatic sulfonates and sulfates on amyloid fibrillogenesis.

Main Results:

Demonstrated a relationship between heparan sulfate proteoglycan, its mRNA, and AA amyloid deposition in vivo.
Showed that heparan sulfate affects the secondary structure of amyloid precursors in vitro, suggesting a role in amyloidogenesis.
Preliminary results indicate that small molecules can inhibit amyloid beta-protein fibrillogenesis and AA amyloidogenesis.

Conclusions:

The interaction between basement membrane proteins and amyloid precursors is a general process in vivo amyloid deposition.
This interaction provides a basis for developing therapeutic strategies against amyloid-based diseases.
Small molecule aliphatic sulfonates and sulfates show promise as therapeutic agents.

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