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Pathogenesis of Alzheimer's Disease Examined Using a Modified Puri-Li Model that Incorporates Calcium Ion Homeostasis
1, 1A, Russell St, Eastwood, NSW 2122, Australia. ranjit@optusnet.com.au.
Journal of Molecular Neuroscience : MN
|May 14, 2018
Summary
Calcium ions play a crucial role in Alzheimer's disease (AD) pathogenesis by enhancing amyloid-beta (Aβ) production and promoting microglia and astroglia proliferation. Controlling calcium levels may offer a therapeutic strategy for AD.
Area of Science:
- Neuroscience
- Computational Biology
- Biochemistry
Background:
- Alzheimer's disease (AD) pathogenesis involves amyloid-beta (Aβ) peptides, microglia, and astroglia.
- Neuronal calcium ion homeostasis is critical in brain function and disease.
Purpose of the Study:
- To investigate the impact of calcium ions on Aβ, microglia, and astroglia in AD pathogenesis.
- To modify the Puri-Li kinetic model to incorporate neuronal calcium ion homeostasis.
Main Methods:
- Solving the modified Puri-Li kinetic model under steady-state conditions.
- Analyzing the derived expressions for Aβ, microglia, and astroglia populations.
Main Results:
- Calcium ions activate Aβ synthesis, creating a positive feedback loop that increases intracellular calcium.
- Calcium ions enhance microglia and astroglia production as AD progresses.
- Microglia and astroglia reach equilibrium by destroying neurons, consistent with AD pathology.
Conclusions:
- Increased calcium ions exacerbate AD by promoting Aβ, microglia, and astroglia.
- The positive feedback loop involving calcium ions and Aβ is a key feature of AD.
- Modulating neuronal calcium levels presents a potential therapeutic avenue for Alzheimer's disease.
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