Abstract
Vascular Dementia (VaD) accounts for nearly 20% of all cases of dementia. eNOS plays an important role in neurovascular remodeling, anti-inflammation, and cognitive functional recovery after stroke. In this study, we investigated whether eNOS regulates brain damage, cognitive function in mouse model of bilateral common carotid artery stenosis (BCAS) induced VaD. Late-adult (6-8 months) C57BL/6J and eNOS knockout (eNOS-/-) mice were subjected to BCAS (n=12/group) or sham group (n=8/group). BCAS was performed by applying microcoils to both common carotid arteries. Cerebral blood flow (CBF) and blood pressure were measured. A battery of cognitive functional tests was performed, and mice were sacrificed 30 days after BCAS. Compared to corresponding sham mice, BCAS in wild-type (WT) and eNOS-/- mice significantly: 1) induces short term, long term memory loss, spatial learning and memory deficits; 2) decreases CBF, increases ischemic cell damage, including apoptosis, white matter (WM) and axonal damage; 3) increases blood brain barrier (BBB) leakage, decreases aquaporin-4 (AQP4) expression and vessel density; 4) increases microglial, astrocyte activation and oxidative stress in the brain; 5) increases inflammatory factor interleukin-1 receptor-associated kinase-1(IRAK-1) and amyloid beta (Aβ) expression in brain; 6) increases IL-6 and IRAK4 expression in brain. eNOS-/-sham mice exhibit increased blood pressure, decreased iNOS and nNOS in brain compared to WT-sham mice. Compared to WT-BCAS mice, eNOS-/-BCAS mice exhibit worse vascular and WM/axonal damage, increased BBB leakage and inflammatory response, increased cognitive deficit, decreased iNOS, nNOS in brain. eNOS deficit exacerbates BCAS induced brain damage and cognitive deficit.
Highlights
Vascular Dementia (VaD) accounts for nearly 20% of all cases of dementia. endothelial nitric oxide synthase (eNOS) plays an important role in neurovascular remodeling, anti-inflammation, and cognitive functional recovery after stroke
Nitric was placed between the loops of the microcoil (the oxide (NO) produced by endothelial nitric oxide synthase microcoils made of piano wire with an inner diameter of has a crucial role in the regulation of systemic 0.16 mm, pitch 0.50 mm, and total length 2.5mm) just blood pressure, vascular tone, vascular remodeling, and below the carotid bifurcation
Reduced cognitive impairment[18]. eNOS plays an important role in CBF is associated with more severe white matter (WM) injury indicated modulating amyloid precursor protein (APP) expression by an animal model employing 0.16mm microcoil on left and microglial activation within the brain and CCA and 0.18mm microcoil on right CCA resulting in cerebrovasculature, and leads to impairment of spatial greater WM injury in the left hemisphere [3]
Summary
A vascular risk factor and a pre-anesthetic, and spontaneously respired with 2%. Genetic inactivation of in our experience, BCAS with 0.16mm eNOS causes activation of microglia and promotes a pro- microcoils induced ~30% mortality at 14 days after BCAS. ENOS plays an important role in CBF is associated with more severe WM injury indicated modulating amyloid precursor protein (APP) expression by an animal model employing 0.16mm microcoil on left and microglial activation within the brain and CCA and 0.18mm microcoil on right CCA resulting in cerebrovasculature, and leads to impairment of spatial greater WM injury in the left hemisphere [3]. Middle aged (14-15 months old) eNOS-/- after 1 month of hypoperfusion, mice with 0.18mm mice have increased APP, amyloid beta levels, microglial microcoils do not exhibit infarctions or hemorrhage in gray activation as well as impaired spatial memory [20]. Induces worse brain damage and cognitive deficit in BCAS the BCAS model with 0.16mm microcoils induces mice
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