Title : Pathogenesis of Alzheimer's Disease Examined Using a Modified Puri-Li Model that Incorporates Calcium Ion Homeostasis.

Pub. Date : 2018 Jun

PMID : 29754213






7 Functional Relationships(s)
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1 The Puri-Li kinetic model is modified to include neuronal calcium ion homeostasis to study the effect of calcium ions on the production of amyloid-beta peptides (Abeta), microglia, and astroglia during the pathogenesis of Alzheimer"s disease (AD). Calcium amyloid beta precursor protein Homo sapiens
2 The derived expressions show that the inclusion of calcium ions has altered the steady-state populations of Abeta, microglia, and astroglia. Calcium amyloid beta precursor protein Homo sapiens
3 The calcium ions activate the synthesis of Abeta which in turn increases the calcium ions entering the cytoplasm of the neuronal cells, thus creating a positive loop. Calcium amyloid beta precursor protein Homo sapiens
4 The calcium ions activate the synthesis of Abeta which in turn increases the calcium ions entering the cytoplasm of the neuronal cells, thus creating a positive loop. Calcium amyloid beta precursor protein Homo sapiens
5 These model results are in agreement with experimental findings, which show a feed back loop between calcium ion levels and Abeta; population increase in microglia, astroglia during AD; and microglia, astroglia acting as inflammatory cells producing toxins to destroy neurons during AD. Calcium amyloid beta precursor protein Homo sapiens
6 Increased production of Abeta, microglia, and astroglia resulting from increased levels of calcium ions suggests that controlling the calcium ion levels could present a therapeutic strategy to combat AD. Calcium amyloid beta precursor protein Homo sapiens
7 Increased production of Abeta, microglia, and astroglia resulting from increased levels of calcium ions suggests that controlling the calcium ion levels could present a therapeutic strategy to combat AD. Calcium amyloid beta precursor protein Homo sapiens