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• W2108797659 abstract "Cerebrovascular dysfunction contributes significantly to the pathoetiology of Alzheimer's disease (AD). Midlife vascular risk factors, such as hypertension, cardiovascular disease, diabetes, and dyslipidemia, increase the relative risk for AD. These comorbidities are all characterized by low and/or dysfunctional high-density lipoproteins (HDL), which itself is a suggested risk factor for AD. In addition to lipid transport, HDL enhances vasorelaxation, reduces inflammation and oxidative stress, and promotes endothelial cell survival and integrity. In mouse models of AD, apolipoprotein (apo) A-I, the primary protein component of HDL, reduces neuroinflammation, suppresses cerebrovascular Aβ deposition, and protects cognitive function, making it an intriguing therapeutic target. However, how apoA-I, which is made only in the liver and intestine yet is present in cerebrospinal fluid (CSF), enters the central nervous system (CNS) is unknown. Endogenous levels of apoA-I in brain, liver, CSF, and plasma were measured by immunoblotting. Recombinant, fluorescently tagged, lipid-free human (h) apoA-I was injected into the tail vein of wild-type mice at doses ranging from 7.5-120mg/kg and tissue was collected 0.5-24h post injection. hapoA-I levels were measured by ELISA. Steady state levels of endogenous murine apoA-I in CSF and brain are approximately 0.01% and 10-15% of its levels in plasma and liver, respectively. hapoA-I delivered via intravenous injection localizes to the choroid plexus within 0.5h and accumulates in a saturable, dose-dependent manner in brain. hapoA-I accumulates in the brain for up to 2h, after which it is turned over with a half-life of ∼133 minutes, 3 times longer than its 40-45 half0-life in plasma, liver, and kidney. In vitro, hapoA-I is taken up, specifically binds to, and is actively transported across confluent monolayers of primary human choroid epithelial cells. As apoA-I mRNA is undetectable in murine brain, apoA-I in the CNS is derived from the circulation. Following intravenous injection, hapoA-I rapidly and strongly localizes to the choroid plexus and can be transported across choroidal epithelial cells in vitro. These results suggest that plasma apoA-I gains access to the CNS primarily via the blood-CSF barrier." @default.
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• W2108797659 date "2014-07-01" @default.
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• W2108797659 title "P1-006: INTRAVENOUSLY INJECTED HUMAN APOLIPOPROTEIN A-I RAPIDLY ENTERS THE CENTRAL NERVOUS SYSTEM VIA THE CHOROID PLEXUS IN MICE" @default.
• W2108797659 doi "https://doi.org/10.1016/j.jalz.2014.05.241" @default.
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