Rex CS, Gavin CF, Rubio MD, Kramar EA, Chen LY, Jia Y, Huganir RL, Muzyczka N, Gall CM, Miller CA, Lynch G, Rumbaugh G.
Myosin IIb regulates actin dynamics during synaptic plasticity and memory formation.
Neuron. 2010 Aug 26;67(4):603-17.
PubMed.
This exciting study demonstrates that the activity of myosin IIB is required for the synthesis of F-actin during long-term potentiation. The authors find that the interactions between actin and myosin II are important for synaptic plasticity and memory consolidation. Although further investigation is needed, the presented results raise the possibility of new therapeutic approaches for the treatment of Alzheimer disease and other memory disorders.
In this context, the evaluation of amyloid-β, performed in the same model system, would be of great interest. Indeed, our group has recently shown that myosin IIB has an influence on the trafficking and processing of amyloid precursor protein, but a limitation of our work is that it has been performed in cultured neurons and not in animal models. If the in vivo perturbation of the actin/myosin II interaction was able to produce amyloid accumulation, then a mechanistic correlation between amyloid-β and memory impairment could be revealed.
Comments
University of Genoa
This exciting study demonstrates that the activity of myosin IIB is required for the synthesis of F-actin during long-term potentiation. The authors find that the interactions between actin and myosin II are important for synaptic plasticity and memory consolidation. Although further investigation is needed, the presented results raise the possibility of new therapeutic approaches for the treatment of Alzheimer disease and other memory disorders.
In this context, the evaluation of amyloid-β, performed in the same model system, would be of great interest. Indeed, our group has recently shown that myosin IIB has an influence on the trafficking and processing of amyloid precursor protein, but a limitation of our work is that it has been performed in cultured neurons and not in animal models. If the in vivo perturbation of the actin/myosin II interaction was able to produce amyloid accumulation, then a mechanistic correlation between amyloid-β and memory impairment could be revealed.
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