Abstract：
:Brain deposits of amyloid beta peptide (Abeta) have been a diagnostic hallmark of Alzheimer's disease (AD) for nearly a century. Recent studies have demonstrated that Abeta is also present in peripheral blood. Here, we present evidence that circulating Abeta42 is subject to complement C3b-dependent adherence to complement receptor 1 (CR1) on erythrocytes, a classical set of mechanisms by which pathogens and proteins recognized as foreign are cleared from the bloodstream. Levels of Abeta42 targeted by this pathway differ significantly in AD compared to mild cognitive impairment and nondemented elderly controls.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Rogers J,Li R,Mastroeni D,Grover A,Leonard B,Ahern G,Cao P,Kolody H,Vedders L,Kolb WP,Sabbagh Mdoi
10.1016/j.neurobiolaging.2005.09.043subject
Has Abstractpub_date
2006-12-01 00:00:00pages
1733-9issue
12eissn
0197-4580issn
1558-1497pii
S0197-4580(05)00313-1journal_volume
27pub_type
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journal_title：Neurobiology of aging
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journal_title：Neurobiology of aging
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journal_title：Neurobiology of aging
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