Adding oligermized amyloid-beta to neurons on MEA?
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Adding oligomerized amyloid-beta to neurons on Microelectrode Arrays (MEAs) can lead to functional deficits in hippocampal neurons. Studies have shown that micromolar concentrations of Aβ 42 oligomers inhibit spontaneous electrical activity of cells, with partial reversibility. Additionally, exposure to oligomeric amyloid-beta can cause functional toxicity by inhibiting firing of hippocampal neurons without significant cell death at low concentrations. This functional deficit can be reversed using curcumin, an inhibitor of Aβ oligomerization. Furthermore, exposure to oligomeric amyloid-beta induces changes in the neuronal proteome and phosphoproteome, affecting proteins related to neurodegeneration. The initial molecular event leading to neuronal damage involves calcium influx induced by oligomers, which can be prevented by specific molecules like clusterin and nanobodies. These findings highlight the impact of oligomerized amyloid-beta on neuronal function and the potential for targeted interventions.
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41 Citations | Not addressed in the paper. |
17 Citations | Exposing neurons to oligomeric amyloid-beta induces early proteomic changes, including altered levels of TDP-43, hnRNPs, COPI proteins, 20S proteasome subunits, VAMP1/2, and tau phosphorylation at serine 208. |
66 Citations | Oligomerized amyloid-beta added to neurons on MEA inhibits firing without cell death, a reversible effect with curcumin, suggesting a new target for Alzheimer's drug development. |
01 Jan 2009 4 Citations | Micromolar concentrations of Aβ 42 oligomers, not fibrils, inhibited hippocampal neuron activity on MEA, indicating synaptotoxicity in Alzheimer's disease research. |
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