Accumulation of Amyloid Beta (Aβ) Peptide on Blood Vessel Walls in the Damaged Brain after Transient Middle Cerebral Artery Occlusion

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.

Bioactivity of Torch Ginger Umbut Extract (Etlingera elatior) Against Heal Wounds of Mice (Mus musculus)

“…Saponins work by stimulating the formation of new cells, or called Growth Factor. Causing the multiplication and growth of blood vessel endothelial cells, vascular smooth muscle cells and fibroblasts, causing cellular growth which ultimately repair damaged blood vessel walls [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34].…”

Destructive Effects of Pyroptosis on Homeostasis of Neuron Survival Associated with the Dysfunctional BBB-Glymphatic System and Amyloid-Beta Accumulation after Cerebral Ischemia/Reperfusion in Rats

“…Furthermore, a clinical study by Liu et al [ 5 ] demonstrated that patients with A β deposition experienced a more severe and rapid cognitive decline over 3 years after stroke/transient ischemic attack compared with subjects without AD-like A β deposition, and A β was associated with changes in multiple cognitive domains. Recently, Martins et al [ 6 ] have reported the acute accumulation of A β oligomers within 24 h in blood vessel walls including small capillaries and nearby brain tissues after cerebral I/R, and that such accumulation acts as a detrimental factor promoting brain damage. Additionally, the accumulation of toxic A β can produce swelling in astrocytes and their endfeet and also cause dysregulation of capillaries by acting on pericytes, influencing energy supply for neurons [ 45 , 46 ].…”

On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications

“…A similar accumulation of Aβ around blood vessels in the skin of AD patients and generally in older patients was described many years ago ( 66 , 139 ). Moreover, we recently reported that Aβ immunofluorescence accumulated on blood vessel walls in the damaged part of the brain and on nearby astrocytes after middle cerebral artery occlusion ( 35 ). Temporary accumulation of Aβ in GFAP-positive astrocytic bodies and processes that formed clusters with specific small vessel-like structures was reported previously ( 29 , 140 – 143 ), see also review: ( 38 ).…”