Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized histopathologically by neuritic plaques of accumulated β-amyloid and cytoskeletal abnormalities. Although a variety of pathological processes have been proposed, including exci-totoxic effects of glutamate and disturbances in Ca2+-homeostasis (1, 2), the mechanisms responsible for this condition remain essentially unknown. We have recently observed a significant decrease in IP3-receptor levels in post mortem brain samples from AD cases compared to matched control material (3). Interestingly, in the same samples, the levels of several other brain proteins including synaptophysin and phosphate-activated glutaminase (PAG), were unchanged.
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Haug, L.S., Østvold, A.C., Torgner, I., Roberg, B., DvoÍáková, L., Walaas, S.I. (1997). Type I Inositol (1,4,5) Trisphosphate Receptor and Phosphate-Activated Glutaminase are Highly Enriched in Neurons as Compared to Glial Cells in Rat Neostriatum. In: Teelken, A., Korf, J. (eds) Neurochemistry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5405-9_65
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DOI: https://doi.org/10.1007/978-1-4615-5405-9_65
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