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Amyloid-β disrupts ongoing spontaneous activity in sensory cortex
Shlomit Beker1, Miri Goldin1, Noa Menkes-Caspi1
1Gonda Brain Research Center, Bar-Ilan University, 52900, Ramat Gan, Israel.
Brain Structure & Function
|December 20, 2014
Summary
Alzheimer's disease pathology alters neuronal activity and network coherence in APP/PS1 mice. This amyloid-beta-induced dysfunction affects individual neurons and network integrity, leading to cortical dysfunction.
Area of Science:
- Neuroscience
- Pathology
- Biomedical Research
Background:
- Alzheimer's disease (AD) pathology's impact on neocortical neuronal activity in intact networks is poorly understood.
- Spontaneous neuronal activity forms the basis for further evoked activity in the neocortex.
Purpose of the Study:
- To investigate the effects of amyloid-beta (Aβ) accumulation on spontaneous neuronal activity and network dynamics in the APP/PS1 mouse model of AD.
- To compare in vivo intracellular recordings and local field potentials (LFP) between transgenic mice and controls.
Main Methods:
- In vivo intracellular recordings and LFP analysis of ongoing neuronal activity in the barrel cortex.
- Comparison of APP/PS1 transgenic mice with age-matched littermate controls exhibiting significant Aβ burden.
- Assessment of neuronal membrane potential dynamics, spiking properties, and neurite morphology.
Main Results:
- Neurons in Aβ-burdened cortex showed altered membrane potential dynamics, including shorter depolarized state durations and failed transitions.
- APP/PS1 neurons exhibited changes in firing patterns and spike shape compared to controls.
- Reduced coherence within neuronal assemblies and altered neurite morphology were observed in APP/PS1 mice, indicating network-level dysfunction.
Conclusions:
- Amyloid-beta accumulation in the brain significantly alters spontaneous neuronal activity at both individual neuron and network levels.
- These alterations contribute to reduced network integrity and widespread cortical dysfunction in the APP/PS1 model.
- The findings suggest a cascade effect where individual neuronal dysfunction amplifies to network-level impairments in Alzheimer's disease.
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