By Suzanne De La Monte
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Extra resources for Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets
The merged image (C) of panels (A) and (B) reveals colocalization of these proteins (yellow).
Data were analyzed using ANOVA and Fisher’s PLSD-test (Stat View®; SAS Institute Inc, Cary, NC. USA). Other data were expressed as mean±SD and analyzed using ANOVA. 05 was considered statistically significant. 3. 1-3). Neurons, astroglia or microglia were identified by immunohistochemical staining using anti-NF, anti-MAP-2, and anti-GFAP or anti-CD11b, respectively. Double labeling immunohistochemistry with anti- 36 Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets NF (Fig.
In a recent study, Zhao and Townsend are demonstrated that insulin resistance and Aβ disrupt common signal transduction cascades including the insulin receptor family/Phosphoinositide 3-kinase/Akt/Glycogen synthase kinase3(GSK3) pathway. They reported that both disease processes contribute to overlapping pathology, thereby compounding disease symptoms and progression (Zhao & Townsend, 2009). The age-associated decline in the metabolic rate and utilization of glucose by the frontal cortex imply that insulin resistance can cause executive dysfunctions in older people, not only global cognitive impairment.
Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets by Suzanne De La Monte