What Have Google’s Random Quantum Circuit Simulation Experiments Demonstrated about Quantum Supremacy?

Quantum computing is of high interest because it promises to perform at least some kinds of computations much faster than classical computers. Arute et al. 2019 (informally, “the Google Quantum Team”) report the results of experiments that purport to demonstrate “quantum supremacy” – the claim that the performance of some quantum computers is better than that of classical computers on some problems. Do these results close the debate over quantum supremacy? We argue that they do not. In the following, we provide an overview of the Google Quantum Team’s experiments, then identify some open questions in the quest to demonstrate quantum supremacy

What Have Google’s Random Quantum Circuit Simulation Experiments Demonstrated about Quantum Supremacy?

Quantum computing is of high interest because it promises to perform at least some kinds of computations much faster than classical computers. Arute et al. 2019 (informally, “the Google Quantum Team”) report the results of experiments that purport to demonstrate “quantum supremacy” – the claim that the performance of some quantum computers is better than that of classical computers on some problems. Do these results close the debate over quantum supremacy? We argue that they do not. In the following, we provide an overview of the Google Quantum Team’s experiments, then identify some open questions in the quest to demonstrate quantum supremacy

Statin therapy inhibits remyelination in the central nervous system

Remyelination of lesions in the central nervous system contributes to neural repair following clinical relapses in multiple sclerosis. Remyelination is initiated by recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating oligodendrocytes. Simvastatin, a blood-brain barrier-permeable statin in multiple sclerosis clinical trials, has been shown to impact the in vitro processes that have been implicated in remyelination. Animals were fed a cuprizone-supplemented diet for 6 weeks to induce localized demyelination in the corpus callosum; subsequent return to normal diet for 3 weeks stimulated remyelination. Simvastatin was injected intraperitoneally during the period of coincident demyelination and OPC maturation (weeks 4 to 6), throughout the entire period of OPC responses (weeks 4 to 9), or during the remyelination-only phase (weeks 7 to 9). Simvastatin treatment (weeks 4 to 6) caused a decrease in myelin load and both Olig2(strong) and Nkx2.2(strong) OPC numbers. Simvastatin treatment (weeks 4 to 9 and 7 to 9) caused a decrease in myelin load, which was correlated with a reduction in Nkx2.2(strong) OPCs and an increase in Olig2(strong) cells, suggesting that OPCs were maintained in an immature state (Olig2(strong)/Nkx2.2(weak)). NogoA+ oligodendrocyte numbers were decreased during all simvastatin treatment regimens. Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes