Abstract
Accumulation of beta amyloid (Aβ) fibrils in senile plaques and cerebral blood vessel walls is characteristic of Alzheimer’s disease (AD). We discuss several models that seek to explain the neurotoxic consequences, in particular the manner in which the neurotoxicity promotes cell dysfunction and cell death by an increase in cytosolic calcium ion concentration. To base correctly a new therapy on in vitro experiments, one must choose the right model mechanism.
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Ingram, V.M. (2005). The Role of Alzheimer Aβ Peptides in Ion Transport Across Cell Membranes. In: Harris, J.R., Fahrenholz, F. (eds) Alzheimer’s Disease. Subcellular Biochemistry, vol 38. Springer, Boston, MA . https://doi.org/10.1007/0-387-23226-5_17
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DOI: https://doi.org/10.1007/0-387-23226-5_17
Publisher Name: Springer, Boston, MA
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