β-Amyloid precursor protein is detectable on monocytes and is increased in Alzheimer’s disease

Using the anti-beta-amyloid precursor protein (βAPP) monoclonal antibodies 4G8, 6E10 and 22C11 and flow cytometry, we report that human circulating peripheral blood monocytes display surface immunoreactivity for βAPP. In contrast, circulating lymphocytes do not possess cell surface βAPP immunoreacti...

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Bibliographic Details
Published in:Neurobiology of aging 1999-05, Vol.20 (3), p.249-257
Main Authors: Jung, Sonia S, Gauthier, Serge, Cashman, Neil R
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Aging
Aging - pathology
Alzheimer Disease - immunology
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer’s disease
Amyloid beta-Protein Precursor - analysis
Amyloid beta-Protein Precursor - immunology
Amyloid beta-Protein Precursor - metabolism
Amyloid precursor protein
Antibody Specificity
Biological and medical sciences
Blotting, Western
Cell surface
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
FACS
Flow Cytometry
Human
Humans
Lymphocytes - chemistry
Macrophages
Medical sciences
Membrane Proteins - analysis
Middle Aged
Monocytes
Monocytes - chemistry
Monocytes - immunology
Monocytes - metabolism
Neurology
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Summary:Using the anti-beta-amyloid precursor protein (βAPP) monoclonal antibodies 4G8, 6E10 and 22C11 and flow cytometry, we report that human circulating peripheral blood monocytes display surface immunoreactivity for βAPP. In contrast, circulating lymphocytes do not possess cell surface βAPP immunoreactivity, despite similar levels of βAPP expression. Immunoblotting analysis showed that monocytes, but not lymphocytes, possess an 82kDa C-terminal βAPP fragment consistent with a processed transmembrane species. Monocyte surface βAPP was upregulated ∼threefold by activation with lipopolysaccharide and interferon-γ; activation did not produce detectable βAPP on the cell surface of lymphocytes. Surface βAPP immunoreactivity was reduced in a normal aged population compared to normal young controls (Young = 81.07 ± 13.67 mean fluorescence units, Aged = 36.74 ± 3.81, p < 0.01), but was significantly increased in AD subjects compared to age-matched healthy controls (AD = 60.31 ± 7.42, p < 0.05). Our data suggest that a proportion of peripheral Aβ may be derived from monocyte/macrophages, and that defects in brain cell processing of βAPP in AD may be shared by this readily accessible peripheral cell.
ISSN:0197-4580
1558-1497
DOI:10.1016/S0197-4580(99)00051-2