Alzheimer’s disease (AD), which accounts for ~70% of dementia cases, shares key mechanisms with late-onset epilepsy, including neuroinflammation and amyloid buildup. Seizures further accelerate Aβ and tau accumulation, worsening cognitive decline, as seen in hAPP-J20 mice.
We conducted a longitudinal study tracking spatial learning, memory loss, and Aβ plaque buildup in Tg and non-Tg mice from birth to 27 weeks. Behavioral tests, immunostaining (NPY, CaMK2, PV), and video-EEG were performed every 3 weeks.
Our results link Aβ deposition to seizure activity, reduced neuronal density, and rising HFOs, especially fast ripples and pathological ripples, highlighting their potential as early biomarkers of epileptogenesis in AD.
Temporal analysis of HFO incidence from chronic CA1 recordings: Ripple (80–200 Hz, top) and fast ripple (250–500 Hz, bottom) rates were similar between nTg and Tg mice before 15 weeks (pre-plaque stage), but showed a significant increase in Tg mice after 17–18 weeks.
Published Paper: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.087939
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