Premium
Plasma β‐Amyloid Peptide, Transforming Growth Factor‐β1, and Risk for Cerebral Amyloid Angiopathy
Author(s) -
GREENBERG STEVEN M.,
CHO HYUNSOON,
O'DONNELL HEATHER C.,
ROSAND JONATHAN,
SEGAL ALAN Z.,
YOUNKIN LINDA H.,
YOUNKIN STEVEN G.,
REBECK G. WILLIAM
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06361.x
Subject(s) - cerebral amyloid angiopathy , pathogenesis , amyloid (mycology) , peptide , apolipoprotein e , apolipoprotein b , medicine , serum amyloid a , amyloidosis , pathology , endocrinology , chemistry , disease , inflammation , biochemistry , dementia , cholesterol
A bstract : Despite the documented association between apolipoprotein E genotype and cerebral amyloid angiopathy (CAA), a substantial proportion of CAA‐related hemorrhages occur in patients without known risks for this disorder. Two other factors implicated in the pathogenesis of CAA are the amyloid‐β peptide (preferentially deposited in vessels as a 40‐amino acid species) and the multifunctional cytokine transforming growth factor‐β1 (a specific promoter of vascular amyloid deposition in transgenic models). We measured plasma concentrations of these factors in a series of 25 patients diagnosed with probable or definite CAA‐related hemorrhage and compared them with 21 patients with hemorrhage due to probable hypertensive vasculopathy and 42 elderly control subjects without hemorrhage. We found no differences among the groups in concentrations of the 40‐ or 42‐amino acid species of β‐amyloid or either the active or latent form of transforming growth factor‐β1. While the data do not exclude important roles for these molecules as risks for CAA, they indicate that plasma measurements are not useful in its diagnosis.