Human plasma semicarbazide sensitive amine oxidase (SSAO), beta-amyloid protein and aging

Semicarbazide sensitive amine oxidase (SSAO) metabolizes oxidative deamination of primary aromatic and aliphatic amines. The final products of its catalysis, ammonia, hydrogen peroxide (H2O2) and the corresponding aldehyde, may contribute to diseases involving vascular degeneration. SSAO is selectively expressed in blood vessels in the brain, but is also present in blood plasma. We have previously reported that membrane-bound SSAO is overexpressed in the cerebrovascular tissue of Alzheimer's disease (AD) patients. The aim of the present work is to study whether the circulating SSAO is also altered in this neurodegenerative disease. SSAO activity was determined in plasma of control cases (n = 23) and patients suffering sporadic Alzheimer dementia, distributed according to the Global Deterioration Scale (GDS): mild (n = 33), moderate (n = 14), moderate-severe (n = 15) and severe dementia (n = 19). Results show a clear increase of plasma SSAO activity (p < 0.001) in moderate-severe and severe AD patients, with patient age being an independent correlative factor. However, plasma SSAO activity was not altered in AD patients with mild or moderate dementia compared to controls. beta-Amyloid (Abeta) (40-42) immunoreactivity in plasma samples was also determined, and no correlation was observed between Abeta 40-42 levels and the severity of the dementia or the plasma SSAO activity. Our results suggest that an increase in circulating SSAO activity could contribute to oxidative stress and vascular damage in advanced Alzheimer's disease.