Rationale and motivation for the model
Our approach to the modeling of the senile plaque growth and further
clustering is based on several experimental observations:
- Although the precursor peptide Abeta is produced uniformly
throughout the cortex of the brain, the aggregated Abeta
deposits are anatomically discrete, roughly spherical clusters
of Abeta fibrils.
- The amount of Abeta is not correlated with the duration or the
severity of the disease, suggesting that after the onset of the
disease the process of plaque formation reaches a dynamic equilibrium.
- Senile plaques as observed under confocal microscope have a very
specific porous yet nonfractal structure.
- Recent experiments suggest that certain agents in the brain interfere
with Abeta aggregation and potentially trigger reversal of Abeta
protein to its nontoxic components.