Tiveci2005 - Calcium dynamics in brain energy metabolism and Alzheimer's disease

Tiveci2005 - Calcium dynamics in brain energy
metabolism and Alzheimer's disease
Encoded non-curated model. Issues:

-
Missing values:
dHb,0 ;

α ; V ; γ ; Volume ; rc ;
V

leak,mem,Ca

; V

Ca,Pump,ER

; V

ch,ER,Ca

;

V

Atpase

- Missing species: Na
+ ; Pr ; CaPr ; Ca

- Confusing values: n = N ; Sm/Vi = S/V ; gna =
g'na ; pscap/Vi = Psc/V

- Confusing rate equations: is it 2.38 or equation
16 in Table 2.1 describing Cai? ; circular dependence on
2.26 

This model is described in the article:

Modelling of calcium
dynamics in brain energy metabolism and Alzheimer's
disease.

Tiveci S, Akin A, Cakir T,
Saybaşili H, Ulgen K.
Comput Biol Chem 2005 Apr; 29(2):
151-162
Abstract:

Functional imaging techniques play a major role in the study
of brain activation by monitoring the changes in blood flow and
energy metabolism. In order to interpret functional
neuroimaging data better, the existing mathematical models
describing the links that may exist between electrical
activity, energy metabolism and hemodynamics in literature are
thoroughly analyzed for their advantages and disadvantages in
terms of their prediction of available experimental data. Then,
these models are combined within a single model that includes
membrane ionic currents, glycolysis, mitochondrial activity,
exchanges through the blood-brain barrier, as well as brain
hemodynamics. Particular attention is paid to the transport and
storage of calcium ions in neurons since calcium is not only an
important molecule for signalling in neurons, but it is also
essential for memory storage. Multiple efforts have underlined
the importance of calcium dependent cellular processes in the
biochemical characterization of Alzheimer's disease (AD),
suggesting that abnormalities in calcium homeostasis might be
involved in the pathophysiology of the disease. The ultimate
goal of this study is to investigate the hypotheses about the
physiological or biochemical changes in health and disease and
to correlate them to measurable physiological parameters
obtained from functional neuroimaging data as in the time
course of blood oxygenation level dependent (BOLD) signal. When
calcium dynamics are included in the model, both BOLD signal
and metabolite concentration profiles are shown to exhibit
temporal behaviour consistent with the experimental data found
in literature. In the case of Alzheimer's disease, the effect
of halved cerebral blood flow increase results in a negative
BOLD signal implying suppressed neural activity.

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