By Suzanne De La Monte
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Extra resources for Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets
2004). , 2004). m. m. during seven consecutive days. Each daily training session consisted of four trials with a 120s cutoff time, followed by 30s rest on the platform. Memory was tested in fifteen animals from each of the anti-APP antibody group and the PBS group, and in ten sham operation group animals, starting at day one and continued up to seven days after TBI/sham operation. 5) in PBS. The brains were then removed and stored in PFA for three days, before the maximum size of the lesion was sliced into serial coronal sections (50μm thick) using a microslicer (Dousaka EM, Kyoto, Japan).
At 7 days after traumatic injury, a few CD11b-positive cells (Fig. 2G) expressed weakly positive APP immunoreactivity (Fig. 2H&I). Fig. 1. Double-immunofluorescence staining of localized neurofilaments (A) or MAP-2 (D) and APP (B, E) around the damaged area after traumatic brain injury. At 1 day after injury, damaged dystrophic and swollen neurites (A, green) in the cortex were APP-positive (B, red). The merged image (C) of panels (A) and (B) reveals colocalization of these proteins (yellow).
2000) Insulin effects on glucose metabolism, memory, and plasma amyloid precursor protein in Alzheimer’s disease differ according to apolipoprotein-E genotype. Ann NY Acad Sci. 903: 222-228. Coleman PD & Yao PJ (2003) Synaptic slaughter in Alzheimer’s disease. Neurobiol Aging. 24:1023–1027. Cuello AC (2007) Overview of the Alzheimer’s Disease Pathology and Potential Therapeutic Targets. Eds: Cuello AC. Pharmacological Mechanisms in Alzheimer’s Therapeutics, Springer, Canada, 1-27. Deane R & Zlokovic BV (2007) Role of the blood-brain barrier in the pathogenesis of Alzheimer’s disease.
Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets by Suzanne De La Monte