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Quantum speedup in the identification of cause-effect relations.

ABSTRACT: The ability to identify cause-effect relations is an essential component of the scientific method. The identification of causal relations is generally accomplished through statistical trials where alternative hypotheses are tested against each other. Traditionally, such trials have been based on classical statistics. However, classical statistics becomes inadequate at the quantum scale, where a richer spectrum of causal relations is accessible. Here we show that quantum strategies can greatly speed up the identification of causal relations. We analyse the task of identifying the effect of a given variable, and we show that the optimal quantum strategy beats all classical strategies by running multiple equivalent tests in a quantum superposition. The same working principle leads to advantages in the detection of a causal link between two variables, and in the identification of the cause of a given variable.

SUBMITTER: Chiribella G

PROVIDER: S-EPMC6443664 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Quantum speedup in the identification of cause-effect relations.

Chiribella Giulio G Ebler Daniel D

Nature communications 20190401 1

The ability to identify cause-effect relations is an essential component of the scientific method. The identification of causal relations is generally accomplished through statistical trials where alternative hypotheses are tested against each other. Traditionally, such trials have been based on classical statistics. However, classical statistics becomes inadequate at the quantum scale, where a richer spectrum of causal relations is accessible. Here we show that quantum strategies can greatly sp ...[more]

PMID: 30931930

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Project description:Late-onset neurodegenerative diseases remain poorly understood as search continues for the perceived pathogenic protein species. Previously, variants in Superoxide Dismutase 1 (SOD1) causing Amyotrophic Lateral Sclerosis (ALS) were found to destabilize and reduce net charge, suggesting a pathogenic aggregation mechanism. This paper reports analysis of compiled patient data and experimental and computed protein properties for variants of human SOD1, a major risk factor of ALS. Both stability and reduced net charge correlate significantly with disease, with larger significance than previously observed. Using two independent methods and two data sets, a probability < 3% (t-statistical test) is found that ALS-causing mutations share average stability with all possible 2907 SOD1 mutations. Most importantly, un-weighted patient survival times correlate strongly with the misfolded/unfolded protein copy number, expressed as an exponential function of the experimental stabilities (R2 = 0.31, p = 0.002), and this phenotype is further aggravated by charge (R2 = 0.51, p = 1.8 x 10-5). This finding suggests that disease relates to the copy number of misfolded proteins. Exhaustion of motor neurons due to expensive protein turnover of misfolded protein copies is consistent with the data but can further explain e.g. the expression-dependence of SOD1 pathogenicity, the lack of identification of a molecular toxic mode, elevated SOD1 mRNA levels in sporadic ALS, bioenergetic effects and increased resting energy expenditure in ALS patients, genetic risk factors affecting RNA metabolism, and recent findings that a SOD1 mutant becomes toxic when proteasome activity is recovered after washout of a proteasome inhibitor. Proteome exhaustion is also consistent with energy-producing mitochondria accumulating at the neuromuscular junctions where ALS often initiates. If true, this exhaustion mechanism implies a complete change of focus in treatment of ALS towards actively nursing the energy state and protein turnover of the motor neurons.

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Quantum speedup in the identification of cause-effect relations.

Publications

Quantum speedup in the identification of cause-effect relations.

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