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Memristive devices with both electrically and optically induced synaptic dynamic behaviors will be crucial to the accomplishment of brain-inspired neuromorphic computing systems, in which the resistive materials and device architectures are two of the most important cornerstones, but still under challenge. Herein, kuramite Cu3SnS4 is newly introduced into poly-methacrylate as the switching medium to construct memristive devices, and the expected high-performance bio-mimicry of diverse optoelectronic synaptic plasticity is demonstrated. In addition to the excellent basic performances, such as stable bipolar resistive switching with On/Off ratio of ∼486, Set/Reset voltage of ∼-0.88/+0.96 V, and good retention feature of up to 104 s, the new designs of memristors possess not only the multi-level controllable resistive-switching memory property but also the capability of mimicking optoelectronic synaptic plasticity, including electrically and visible/near-infrared light-induced excitatory postsynaptic currents, short-/long-term memory, spike-timing-dependent plasticity, long-term plasticity/depression, short-term plasticity, paired-pulse facilitation, and “learning-forgetting-learning” behavior as well. Predictably, as a new class of switching medium material, such proposed kuramite-based artificial optoelectronic synaptic device has great potential to be applied to construct neuromorphic architectures in simulating human brain functions.

© 2023 Author(s). Published under an exclusive license by AIP Publishing.

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BOSTON — There currently is no cure for Parkinson’s disease, but scientists may have discovered a potential path to slow or stop the disease. Parkinson’s disease is a brain disorder that can cause movement problems such as tremors, poor balance, and walking difficulties, and it can also impair cognitive function. There is no cure and treatments aim to simply reduce symptoms. But a new study in mice by researchers at Johns Hopkins offers new hope. They found that the interaction of two proteins is key to the buildup of protein clumps in the brain that damage healthy brain cells in Parkinson’s. They also suggest that disrupting these proteins with a drug already approved by the FDA to treat cancer could potentially slow or stop the brain damage associated with Parkinson’s. The next step would be to conduct clinical trials in humans, but that will take time.

Motaman, S., Ghafouri, T. & Manavizadeh, N. Sci Rep 14, 10,691 (2024). https://doi.org/10.1038/s41598-024-61224-x.

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