1. Accumulation of Amyloid Beta (Aβ) Peptide on Blood Vessel Walls in the Damaged Brain after Transient Middle Cerebral Artery Occlusion.
- Author
-
Martins AH, Zayas-Santiago A, Ferrer-Acosta Y, Martinez-Jimenez SM, Zueva L, Diaz-Garcia A, and Inyushin M
- Subjects
- Amyloid beta-Peptides antagonists & inhibitors, Animals, Blood Vessels drug effects, Blood Vessels metabolism, Brain drug effects, Brain pathology, Female, Infarction, Middle Cerebral Artery drug therapy, Infarction, Middle Cerebral Artery pathology, Inflammation drug therapy, Inflammation metabolism, Inflammation pathology, Male, Rats, Rats, Sprague-Dawley, Tromethamine pharmacology, Amyloid beta-Peptides metabolism, Blood Vessels chemistry, Brain metabolism, Infarction, Middle Cerebral Artery metabolism
- Abstract
It is well known that amyloid beta (Aβ) peptides are generated in blood vessels, released into the brain during thrombosis, and temporarily accumulate in this organ after injury. Here we demonstrate that 24 h after transient middle cerebral artery occlusion (tMCAO), one of the standard models of focal ischemic stroke, Aβ peptide accumulates in the brain, concentrating on the blood vessel walls. Because Aβ oligomers are known to induce significant damage to brain cells, they act as an additional damaging factor during ischemic stroke. Considering that they have been shown to form ion channels in cells, affecting osmotic balance, we used an Aβ peptide channel blocker, tromethamine (2-amino-2-(hydroxymethyl) propane-1,3-diol), to prevent this additional injury. Tromethamine injected 0.1 g/100 g body weight intraperitoneally at 5 min before tMCAO decreased water content in the damaged hemisphere, as measured by dry brain weight. Congo red staining, which binds only to Aβ oligomer plaques (amyloid), showed that there was no significant presence of plaques. Therefore, we suggest that Aβ peptide oligomers are responsible for some of the brain damage during stroke and that blockage of the ion channels that they form could be beneficial in treating this complex neurological syndrome.
- Published
- 2019
- Full Text
- View/download PDF