Although the causal role of Amyloid-β (Aβ) in Alzheimer's disease (AD) is unclear, it is still
reasonable to expect that lowering concentrations of Aβ in the brain may decrease the risk of …

Background The accumulation, aggregation and deposition of amyloid-β (Aβ) peptides in
the brain are central to the pathogenesis of Alzheimer's disease (AD). Alzheimer's disease …

The N-terminal amino acid 1–83 fragment of apolipoprotein AI (apoA-I) has a strong
propensity to form amyloid fibrils at physiological neutral pH. Because apoA-I has an ability …

Human apolipoprotein AI (apoA-I)-derived amyloidosis can present with either wild-type (Wt)
protein deposits in atherosclerotic plaques or as a hereditary form in which apoA-I variants …

The apolipoprotein E4 allele (APOE4) contributes to Alzheimer's disease (AD) risk and
APOE2 is protective, but the relevant cellular mechanisms are unknown. We have used flow …

The formation of amyloid and other protein deposits in vivo is synonymous with many
pathological conditions such as Alzheimer's disease, Creutzfeldt-Jakob disease and …

The involvement of transporters located at the blood-brain barrier (BBB) has been
suggested in the control of cerebral Aβ levels, and thereby in Alzheimer's disease (AD) …

Apolipoprotein E4 (apoE4), the leading genetic risk factor for Alzheimer's disease (AD), is
less lipidated compared to the most common and AD-benign allele, apoE3. We have …

Amyloid-β (Aβ) plaques is one of the typical pathological hallmark of Alzheimer disease
(AD). Accumulating evidence suggests that the imbalance between Aβ production and …

A number of naturally occurring mutations of apolipoprotein (apo) AI, the major protein of
HDL, are known to be associated with hereditary amyloidosis and atherosclerosis. Here, we …