amyloid prealbumin

04/01/1997 - "In an attempt to establish an animal model of TTR Met-30-associated homozygous familial amyloidotic polyneuropathy and to study the structural and functional properties of human TTR Met 30, we generated a mouse line carrying a null mutation at the endogenous ttr locus (ttr-/-) and the human mutant ttr gene (6.0-hMet 30) as a transgene. "
04/01/2009 - "The search for TTR Met 30 was positive, confirming the diagnosis of familial amyloidotic polyneuropathy. "
09/01/2000 - "Pathology of familial amyloidotic polyneuropathy with TTR met 30 in Kumamoto, Japan."
05/16/2000 - "It is essential to do TTR met 30 analysis in all patients with peripheral polyneuropathy in whom there is obviously a dysautonomic component and no known family history."
05/16/2000 - "[The importance of TTR met 30 in the diagnosis of familial amyloidotic polyneuropathy in the absence of a positive family history]."

08/08/2000 - "Anticipation in early- but not late-onset familial amyloid polyneuropathy (TTR met 30) in Japan."
08/01/1999 - "Two pairs of proven monozygotic twins discordant for familial amyloid neuropathy (FAP) TTR Met 30."
03/01/1993 - "Late-onset familial amyloid polyneuropathy with the TTR Met 30 mutation in France."

11/01/1995 - "In familial amyloidosis resulting from deposition of TTR Met 30 (Swedish-type familial amyloidosis), full-length TTR molecules (some mutant) usually predominate, and TTR fragments lacking three of the eight beta-strands (nonmutant) form a major part of the fibril in senile systemic amyloidosis. "
09/01/1995 - "The most frequent transthyretin (TTR) variant associated with hereditary amyloidosis is TTR Met 30, which has its major focus in Portugal, although it also occurs in many other countries. "

10/01/1996 - "In summary, the clinical presentation of TTR Met 30 mutation is more varied than previously suspected, and leptomeningeal amyloidosis should be considered in the differential diagnosis of obscure conditions involving meninges."
11/01/1995 - "In familial amyloidosis resulting from deposition of TTR Met 30 (Swedish-type familial amyloidosis), full-length TTR molecules (some mutant) usually predominate, and TTR fragments lacking three of the eight beta-strands (nonmutant) form a major part of the fibril in senile systemic amyloidosis. "

10/01/1999 - "This report presents a patient with late-onset TTR-Met 30 who primarily developed amyloid cardiomyopathy, with less amyloid polyneuropathy in the peripheral nervous system than is usually seen. "