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Alzheimer�s disease (AD) diff
ers from other forms of dementia in its relation to
amyloid beta peptide (Abeta42). Abeta42, a proteolytic product of amyloid precursor proteins
(APP), has a toxic eff
ect on neuronal cells. Th
ect implies that protein expression is changed
in neuronal cells by Abeta42, which provides a molecular marker for this disease. In the present
study, we used the mice primary culture neurons and investigated the proteins in the supernatant
er incubation with or without Abeta
In view of the appearance of an acidic phospholipid (phosphatidylserine (PS)) on
the outer plasma membrane of an apoptotic cell, we used PS as a probe and proteins bound to
PS-coated magnetic nano-beads in a Ca
-dependent manner were identifi
ed using a proteomic
Of a number of proteins identifi
ed, we focused on annexin A5 and milk fat globule-
EGF-factor 8 (MFG-E8) that is involved in the clearance of apoptotic cells. Both annexin A5
and MFG-E8 were found to be increased signifi
cantly in the culture supernatant by Abeta42.
Tg2576 mice (AD mouse model), which overexpress mutant human APP, showed signifi
increase of annexin A5 in both the brain cortex and plasma, compared with control. Th
e level of
annexin A5 signifi
cantly increased in a greater proportion of AD patients as compared to that in
a control group (
-value of less than 0.0001 in the logistic regression analysis).
Both annexin A5 and MFG-E8 are novel plasma biomarker candidates for AD
Hitoshi Sohma completed his Ph.D. in biochemistry at Hokkaido University, Japan, focusing on Ca2+-signaling in cell-cell communications, and his postdoctoral studies at the National Institute of Mental Health, NIH. He is a professor in the Department of Educational Development, Sapporo Medical University Center for Medical Education, Sapporo, Japan. He is now involved in both pathobiochemical research and the management of medical education at the university. He has published more than 50 papers in the bio-medical field.
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