Abstract:
:Brain injury increases the risk of Alzheimer's disease (AD) through unknown mechanisms. We studied deposition of amyloid-beta protein (Abeta) in cells exposed to transforming growth factor beta1 (TGFbeta1), a cytokine that regulates cell metabolism during brain injury, and apolipoproteinE (apoE), the major lipid transporter in the brain. The studies were conducted by using brain vascular smooth muscle cells that are engaged in beta-amyloidosis in vivo and produce Abeta in cell culture. We found that cell treatment with TGFbeta1 together with apoE4 strongly increased the amount of cellular Abeta. The intracellular Abeta co-localized with apoE but not with TGFbeta, similarly as in vascular beta-amyloid. Some cellular Abeta/apoE deposits increased in size and persisted in culture even after the TGFbeta1 and apoE4 were removed. The appearance of cellular deposits of Abeta was associated with increased production of the amyloid-beta precursor protein and cellular retention of its mature form. The results suggest that the concomitant presence of apoE and TGFbeta1 can trigger vascular beta-amyloidosis by inducing intracellular formation of stable Abeta/apoE deposits.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Mazur-Kolecka B,Frackowiak J,Le Vine H 3rd,Haske T,Evans L,Sukontasup T,Golabek Adoi
10.1016/s0197-4580(02)00095-7subject
Has Abstractpub_date
2003-03-01 00:00:00pages
355-64issue
2eissn
0197-4580issn
1558-1497pii
S0197458002000957journal_volume
24pub_type
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