Overexpression of semicarbazide sensitive amine oxidase in the cerebral blood vessels in patients with Alzheimer’s disease and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

• Published in: Neuroscience letters Vol. 321; no. 1; pp. 21 - 24
• Main Authors: Ferrer, I., Lizcano, J.M., Hernández, M., Unzeta, M.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 15.03.2002; Elsevier
• Subjects: Aged; Aged, 80 and over; Alzheimer disease; Alzheimer Disease - enzymology; Alzheimer Disease - physiopathology; Amine Oxidase (Copper-Containing) - metabolism; Amyloid beta-Peptides - metabolism; Biological and medical sciences; Blood Vessels - enzymology; Blood Vessels - pathology; Blood Vessels - physiopathology; Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; Cerebral blood vessels; Cerebral Cortex - blood supply; Cerebral Cortex - enzymology; Cerebral Cortex - physiopathology; Cu/Zn superoxide dismutase 1; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Dementia, Multi-Infarct - enzymology; Dementia, Multi-Infarct - physiopathology; Female; Humans; Immunohistochemistry; Male; Medical sciences; Neurology; Oxidative stress; Oxidative Stress - physiology; Semicarbazide sensitive amine oxidase; Up-Regulation - physiology; βA4 Amyloid; Oxidative stress; Semicarbazide sensitive amine oxidase; Alzheimer disease; Cerebral blood vessels; Cu/Zn superoxide dismutase 1; Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; βA4 Amyloid; Human; Nervous system diseases; Enzyme; Central nervous system; Gene overexpression; Cerebral disorder; β Amyloid protein; Blood vessel; Central nervous system disease; CADASIL syndrome; Degenerative disease; Circulatory system; Brain (vertebrata)
• DOI: 10.1016/S0304-3940(01)02465-X
• ISSN: 0304-3940

Semicarbazide sensitive amine oxidase (SSAO) metabolizes oxidative deamination of primary aromatic and aliphatic amines, and, in the brain, it is selectively expressed in blood vessels. SSAO expression is examined, by immunohistochemistry with a purified polyclonal antibody to SSAO from bovine lung, in the brains of subjects with Alzheimer disease (AD; n=10), cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL; n=2), and age-matched controls ( n=8). SSAO immunoreactivity is restricted to meningeal and parenchymal blood vessels in control and diseased brains. Yet, a marked and selective increase in SSAO immunoreactivity occurs in association with βA4 vascular amyloid deposits in patients with AD, and in the vicinity of the typical granular deposits in the blood vessels of gray and white matter in patients with CADASIL. Oxidative deamination of primary aromatic and aliphatic amines by SSAO produces ammonia, hydrogen peroxide and the corresponding aldehyde. Moreover, increased SSAO immunoreactivity is associated with increased Cu/Zn superoxide dismutase 1 expression restricted to abnormal blood vessels in diseased brains. Therefore, it is suggested that increased SSAO expression is a source of oxidative stress in the blood vessel wall in AD and CADASIL.