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Abstract
Accumulated neurotoxicity, defined as the time integral of Aβ oligomer concentration, is proposed as a biomarker for neuronal aging.
- A relationship between biological age and accumulated neurotoxicity is indicated.
- The model links biological and calendar ages of neurons through a new analytical solution.
- Increased half-lives of Aβ monomers and oligomers with age may accelerate biological aging.
- Reducing Aβ monomer production could slow biological aging, showing a linear relationship.
- Biological age is dependent on the half-deposition time of Aβ oligomers into senile plaques.
- Biological age is irreversible, suggesting that plaque-clearing therapies may not reverse cognitive impairment.
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