By a News Reporter-Staff News Editor at Health & Medicine Week -- Investigators publish new report on Neurology. According to news reporting from Shanghai, People's Republic of China, by NewsRx journalists, research stated, "Amyloid-beta (A beta) accumulation in the brain is believed to play a central role in Alzheimer's disease (AD) pathogenesis, and the common late-onset form of AD is characterized by an overall impairment in A beta clearance. Therefore, development of nanomedicine that can facilitate A beta clearance represents a promising strategy for AD intervention."
The news correspondents obtained a quote from the research from Fudan University, "However, previous work of this kind was concentrated at the molecular level, and the disease-modifying effectiveness of such nanomedicine has not been investigated in clinically relevant biological systems. Here, we hypothesized that a biologically inspired nanostructure, apolipoprotein E3-reconstituted high density lipoprotein (ApoE3-rHDL), which presents high binding affinity to A beta might serve as a novel nanomedicine for disease modification in AD by accelerating A beta clearance. Surface plasmon resonance, transmission electron microscopy, and co-immunoprecipitation analysis showed that ApoE3-rHDL demonstrated high binding affinity to both A beta monomer and oligomer. It also accelerated the microglial, astroglial, and liver cell degradation of A beta by facilitating the lysosomal transport. One hour after intravenous administration, about 0.4% ID/g of ApoE3-rHDL gained access to the brain. Four-week daily treatment with ApoE3-rHDL decreased A beta deposition, attenuated microgliosis, ameliorated neurologic changes, and rescued memory deficits in an AD animal model."
According to the news reporters, the research concluded: "The findings here provided the direct evidence of a biomimetic nanostructure crossing the blood brain barrier, capturing A beta and facilitating its degradation by glial cells, indicating that ApoE3-rHDL might serve as a novel nanomedicine for disease modification in AD by accelerating A beta clearance, which also justified the concept that nanostructures with A beta-binding affinity might provide a novel nanoplatform for AD therapy."
For more information on this research see: Lipoprotein-Based Nanoparticles Rescue the Memory Loss of Mice with Alzheimer's Disease by Accelerating the Clearance of Amyloid-Beta. ACS Nano, 2014;8(3):2345-2359. ACS Nano can be contacted at: Amer Chemical Soc, 1155 16TH St, NW, Washington, DC 20036, USA. (American Chemical Society - www.acs.org; ACS Nano - www.pubs.acs.org/journal/ancac3)
Our news journalists report that additional information may be obtained by contacting Q.X. Song, Fudan University, Sch Pharm, PLA, Shanghai 201203, People's Republic of China. Additional authors for this research include M. Huang, L. Yao, X.L. Wang, X. Gu, J. Chen, J. Chen, J.L. Huang, Q.Y. Hu, T. Kang, Z.X. Rong, H. Qi, G. Zheng, H.Z. Chen and X.L. Gao (see also Neurology).
Keywords for this news article include: Asia, Lipids, Shanghai, Neurology, Lipoproteins, Nanomedicine, Nanoparticle, Nanotechnology, Memory Disorders, Emerging Technologies, People's Republic of China
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