Research reports on Alzheimer disease from J. Maeda and colleagues provide new insights
2008 JAN 16 -- According to recent research from Chiba, Japan, "We provide the first evidence for the capability of a high-resolution positron emission tomographic ( PET) imaging system in quantitatively mapping amyloid accumulation in living amyloid precursor protein transgenic (Tg) mice. After the intravenous administration of N-[C-11] methyl-2-(4'-methylaminophenyl)-6-hydroxybenzothiazole ( or [C-11] PIB for ''Pittsburgh Compound-B'') with high-specific radioactivity, the Tg mice exhibited high-level retention of radioactivity in amyloid-rich regions." "PET investigation for Tg mice over an extended range of ages, including longitudinal assessments, demonstrated age-dependent increase in radioligand binding consistent with progressive amyloid accumulation. Reduction in amyloid levels in the hippocampus of Tg mice was also successfully monitored by multiple PET scans along the time course of anti-amyloid treatment using an antibody against amyloid beta peptide (A beta). Moreover, PET scans with [F-18]fluoroethyl-DAA1106, a radiotracer for activated glia, were conducted for these individuals parallel to amyloid imaging, revealing treatment-induced neuroinflammatory responses, the magnitude of which intimately correlated with the levels of pre-existing amyloid estimated by [C-11]PIB. It is also noteworthy that the localization and abundance of [ 11C] PIB autoradiographic signals were closely associated with those of N- terminally truncated and modified A beta, A beta N3-pyroglutamate, in Alzheimer's disease ( AD) and Tg mouse brains, implying that the detectability of amyloid by [ 11C] PIB positron emission tomography is dependent on the accumulation of specific A beta subtypes," wrote J. Maeda and colleagues. The researchers concluded: "Our results support the usefulness of the small animal-dedicated PET system in conjunction with high-specific radioactivity probes and appropriate Tg models not only for clarifying the mechanistic properties of amyloidogenesis in mouse models but also for preclinical tests of emerging diagnostic and therapeutic approaches to AD." Maeda and colleagues published their study in the Journal of Neuroscience (Longitudinal, quantitative assessment of amyloid, neuroinflammation, and anti-amyloid treatment in a living mouse model of Alzheimer's disease enabled by positron emission tomography. Journal of Neuroscience, 2007;27(41):10957-10968). For additional information, contact M. Higuchi, National Institute Radiol Science, Molecular Imaging Center, Inage Ku, 4-9-1 Anagawa, Chiba 2638555, Japan. Publisher contact information for the Journal of Neuroscience is: Society Neuroscience, 11 Dupont Circle, NW, Ste. 500, Washington, DC 20036, USA. Keywords: Japan, Chiba, Alzheimer Disease, Biological Therapy, Immunotherapy, Inflammation, Neuroinflammation, Neuroscience, Treatment. This article was prepared by Immunotherapy Weekly editors from staff and other reports. Copyright 2008, Immunotherapy Weekly via NewsRx.com.
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