R. Pluta et al., EVIDENCE OF BLOOD-BRAIN-BARRIER PERMEABILITY LEAKAGE FOR CIRCULATING HUMAN ALZHEIMERS BETA-AMYLOID-(1-42)-PEPTIDE/, NeuroReport, 7(7), 1996, pp. 1261-1265
BRAINS from patients with Alzheimer's disease contain amyloid plaques
which are composed of beta-amyloid peptide and are considered to play
a causal role in the neuropathology of this disease. The origin of bet
a-amyloid peptide in brain parenchyma and vessels of Alzheimer's disea
se patients is not known. This study examined the permeability of the
blood-brain barrier to beta-amyloid peptide in rats subjected to singl
e or repeated episodes of global cerebral ischaemia followed by i.v. i
njections of human synthetic beta-amyloid-(1-42)-peptide. Rats receivi
ng beta-amyloid peptide after ischaemia demonstrated multifocal and wi
despread accumulation of beta-amyloid peptide in hippocampus, cerebral
cortex and occasionally in white matter. beta-Amyloid peptide penetra
tion involved arterioles, veins and venules. Neuronal, glial and peric
yte bodies were observed filled with beta-amyloid peptide. Direct evid
ence that soluble human beta-amyloid-(1-42)-peptide crosses the blood-
brain barrier and enters the brain from the circulation is thus provid
ed for the first time.