[HTML][HTML] Apolipoprotein AI deficiency increases cerebral amyloid angiopathy and cognitive deficits in APP/PS1ΔE9 mice
I Lefterov, NF Fitz, AA Cronican, A Fogg… - Journal of Biological …, 2010 - ASBMB
A hallmark of Alzheimer disease (AD) is the deposition of amyloid β (Aβ) in brain
parenchyma and cerebral blood vessels, accompanied by cognitive decline. Previously, we
showed that human apolipoprotein AI (apoA-I) decreases Aβ 40 aggregation and toxicity.
Here we demonstrate that apoA-I in lipidated or non-lipidated form prevents the formation of
high molecular weight aggregates of Aβ 42 and decreases Aβ 42 toxicity in primary brain
cells. To determine the effects of apoA-I on AD phenotype in vivo, we crossed APP/PS1ΔE9 …
parenchyma and cerebral blood vessels, accompanied by cognitive decline. Previously, we
showed that human apolipoprotein AI (apoA-I) decreases Aβ 40 aggregation and toxicity.
Here we demonstrate that apoA-I in lipidated or non-lipidated form prevents the formation of
high molecular weight aggregates of Aβ 42 and decreases Aβ 42 toxicity in primary brain
cells. To determine the effects of apoA-I on AD phenotype in vivo, we crossed APP/PS1ΔE9 …
