P
Per Westermark
Researcher at Uppsala University
Publications - 340
Citations - 25299
Per Westermark is an academic researcher from Uppsala University. The author has contributed to research in topics: Amyloid & Amyloidosis. The author has an hindex of 77, co-authored 337 publications receiving 23136 citations. Previous affiliations of Per Westermark include University of Oslo & Linköping University.
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Journal ArticleDOI
Amyloid fibrils in human insulinoma and islets of Langerhans of the diabetic cat are derived from a neuropeptide-like protein also present in normal islet cells.
Per Westermark,Christer Wernstedt,Erik Wilander,David W. Hayden,Timothy O'Brien,Kenneth H. Johnson +5 more
TL;DR: It is suggested that this pancreatic neuropeptide-like protein may exert an important endocrine regulatory effect and be raised to a synthetic human insulinoma IAPP-(7-17) undecapeptide and showed specific immunohistochemical reactivity with human and cat islet amyloid and with islet B cells.
Journal ArticleDOI
Islet Amyloid Polypeptide, Islet Amyloid, and Diabetes Mellitus
TL;DR: This review deals both with physiological aspects of IAPP and with the pathophysiological role of aggregated forms of I APP, including mechanisms whereby human IAPP forms toxic aggregates and amyloid fibrils.
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Islet amyloid polypeptide: pinpointing amino acid residues linked to amyloid fibril formation.
TL;DR: It is concluded that the sequence Ala-Ile-Leu-Ser-Ser, corresponding to positions 25-29 of human IAPP, is strongly amyloidogenic and that a proline-for-serine substitution in position 28, as in several rodents, almost completely inhibits formation of amyloids fibrils.
Journal ArticleDOI
Fibril in senile systemic amyloidosis is derived from normal transthyretin.
TL;DR: It is shown that the TTR molecule in SSA, on the other hand, has a normal primary structure, and factors other than the primary structure of TTR must therefore be important in the pathogenesis of T TR-derived amyloid.
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Islet amyloid: a critical entity in the pathogenesis of type 2 diabetes.
TL;DR: Interventions to prevent islet amyloid formation are emerging, with peptide and small molecule inhibitors being developed that could lead to a preservation of beta-cell mass and amelioration of the islet lesion in type 2 diabetes.