The ability to engineer parallel, programmable operations between desired qubits within a quantum processor is key for building scalable quantum information systems
. In most state-of-the-art ...approaches, qubits interact locally, constrained by the connectivity associated with their fixed spatial layout. Here we demonstrate a quantum processor with dynamic, non-local connectivity, in which entangled qubits are coherently transported in a highly parallel manner across two spatial dimensions, between layers of single- and two-qubit operations. Our approach makes use of neutral atom arrays trapped and transported by optical tweezers; hyperfine states are used for robust quantum information storage, and excitation into Rydberg states is used for entanglement generation
. We use this architecture to realize programmable generation of entangled graph states, such as cluster states and a seven-qubit Steane code state
. Furthermore, we shuttle entangled ancilla arrays to realize a surface code state with thirteen data and six ancillary qubits
and a toric code state on a torus with sixteen data and eight ancillary qubits
. Finally, we use this architecture to realize a hybrid analogue-digital evolution
and use it for measuring entanglement entropy in quantum simulations
, experimentally observing non-monotonic entanglement dynamics associated with quantum many-body scars
. Realizing a long-standing goal, these results provide a route towards scalable quantum processing and enable applications ranging from simulation to metrology.
Motivated by far-reaching applications ranging from quantum simulations of complex processes in physics and chemistry to quantum information processing
, a broad effort is currently underway to build ...large-scale programmable quantum systems. Such systems provide insights into strongly correlated quantum matter
, while at the same time enabling new methods for computation
and metrology
. Here we demonstrate a programmable quantum simulator based on deterministically prepared two-dimensional arrays of neutral atoms, featuring strong interactions controlled by coherent atomic excitation into Rydberg states
. Using this approach, we realize a quantum spin model with tunable interactions for system sizes ranging from 64 to 256 qubits. We benchmark the system by characterizing high-fidelity antiferromagnetically ordered states and demonstrating quantum critical dynamics consistent with an Ising quantum phase transition in (2 + 1) dimensions
. We then create and study several new quantum phases that arise from the interplay between interactions and coherent laser excitation
, experimentally map the phase diagram and investigate the role of quantum fluctuations. Offering a new lens into the study of complex quantum matter, these observations pave the way for investigations of exotic quantum phases, non-equilibrium entanglement dynamics and hardware-efficient realization of quantum algorithms.
Quantum phase transitions (QPTs) involve transformations between different states of matter that are driven by quantum fluctuations
. These fluctuations play a dominant part in the quantum critical ...region surrounding the transition point, where the dynamics is governed by the universal properties associated with the QPT. Although time-dependent phenomena associated with classical, thermally driven phase transitions have been extensively studied in systems ranging from the early Universe to Bose-Einstein condensates
, understanding critical real-time dynamics in isolated, non-equilibrium quantum systems remains a challenge
. Here we use a Rydberg atom quantum simulator with programmable interactions to study the quantum critical dynamics associated with several distinct QPTs. By studying the growth of spatial correlations when crossing the QPT, we experimentally verify the quantum Kibble-Zurek mechanism (QKZM)
for an Ising-type QPT, explore scaling universality and observe corrections beyond QKZM predictions. This approach is subsequently used to measure the critical exponents associated with chiral clock models
, providing new insights into exotic systems that were not previously understood and opening the door to precision studies of critical phenomena, simulations of lattice gauge theories
and applications to quantum optimization
.
Individual neutral atoms excited to Rydberg states are a promising platform for quantum simulation and quantum information processing. However, experimental progress to date has been limited by short ...coherence times and relatively low gate fidelities associated with such Rydberg excitations. We report progress towards high-fidelity quantum control of Rydberg-atom qubits. Enabled by a reduction in laser phase noise, our approach yields a significant improvement in coherence properties of individual qubits. We further show that this high-fidelity control extends to the multi-particle case by preparing a two-atom entangled state with a fidelity exceeding 0.97(3), and extending its lifetime with a two-atom dynamical decoupling protocol. These advances open up new prospects for scalable quantum simulation and quantum computation with neutral atoms.
The realization of large-scale fully controllable quantum systems is an exciting frontier in modern physical science. We use atom-by-atom assembly to implement a platform for the deterministic ...preparation of regular one-dimensional arrays of individually controlled cold atoms. In our approach, a measurement and feedback procedure eliminates the entropy associated with probabilistic trap occupation and results in defect-free arrays of more than 50 atoms in less than 400 milliseconds. The technique is based on fast, real-time control of 100 optical tweezers, which we use to arrange atoms in desired geometric patterns and to maintain these configurations by replacing lost atoms with surplus atoms from a reservoir. This bottom-up approach may enable controlled engineering of scalable many-body systems for quantum information processing, quantum simulations, and precision measurements.
One of the most common symptoms of Alzheimer's disease (AD) and related tauopathies is memory loss. The exact mechanisms leading to memory loss in tauopathies are not yet known; however, decreased ...translation due to ribosomal dysfunction has been implicated as a part of this process. Here we use a proteomics approach that incorporates subcellular fractionation and coimmunoprecipitation of tau from human AD and non-demented control brains to identify novel interactions between tau and the endoplasmic reticulum (ER). We show that ribosomes associate more closely with tau in AD than with tau in control brains, and that this abnormal association leads to a decrease in RNA translation. The aberrant tau-ribosome association also impaired synthesis of the synaptic protein PSD-95, suggesting that this phenomenon contributes to synaptic dysfunction. These findings provide novel information about tau-protein interactions in human brains, and they describe, for the first time, a dysfunctional consequence of tau-ribosome associations that directly alters protein synthesis. Significance statement: Despite the identification of abnormal tau-ribosomal interactions in tauopathies >25 years ago, the consequences of this association remained elusive until now. Here, we show that pathological tau associates closely with ribosomes in AD brains, and that this interaction impairs protein synthesis. The overall result is a stark reduction of nascent proteins, including those that participate in synaptic plasticity, which is crucial for learning and memory. These data mechanistically link a common pathologic sign, such as the appearance of pathological tau inside brain cells, with cognitive impairments evident in virtually all tauopathies.
This book offers an accessibly written introduction to ALS, focusing on the topics that matter most to anyone whose life has been affected-directly or indirectly-by this condition.Amyotrophic lateral ...sclerosis (ALS) or Lou Gehrig's disease, is a neurodegenerative disease that affects the motor neurons that drive voluntary movement. Those diagnosed with ALS experience difficulty moving and speaking and, as the condition worsens, difficulty swallowing and breathing. Beyond this definition, however, what do those affected by ALS need to know?What You Need to Know about ALS is a part of Greenwood's Inside Diseases and Disorders series. This series profiles a variety of physical and psychological conditions, and distills vast collections of scientific knowledge into concise, readable volumes. A list of "Top 10" essential questions begins each book, providing quick-access answers to readers' concerns. The text follows a standardized structure, with each chapter exploring a particular facet of the topic. In addition to covering causes, signs and symptoms, diagnosis, and treatment options, books in this series delve into issues that are less commonly addressed but still critical to understand, such as effects on loved ones and caregivers. Case illustrations highlight key themes discussed in the book and are accompanied by insightful analyses and recommendations. Approaches the subject in a holistic manner, covering often-overlooked areas such as societal perceptions and impacts on family and friends Provides quick answers to the questions that readers are most likely to have in an Essential Questions section that also serves as a springboard for understanding the content of the book in greater depth Provides relatable, real-world examples of concepts discussed in Case Illustrations Points readers toward useful books, organizations, and websites in an annotated Directory of Resources guiding further study and research
With advancing age, the brain becomes increasingly susceptible to neurodegenerative diseases, most of which are characterized by the misfolding and errant aggregation of certain proteins. The ...induction of aggregation involves a crystallization-like seeding mechanism by which a specific protein is structurally corrupted by its misfolded conformer. The latest research indicates that, once formed, proteopathic seeds can spread from one locale to another via cellular uptake, transport, and release. Impeding this process could represent a unified therapeutic strategy for slowing the progression of a wide range of currently intractable disorders.
Neutral-atom arrays have recently emerged as a promising platform for quantum information processing. One important remaining roadblock for the large-scale application of these systems is the ability ...to perform error-corrected quantum operations. To entangle the qubits in these systems, atoms are typically excited to Rydberg states, which could decay or give rise to various correlated errors that cannot be addressed directly through traditional methods of fault-tolerant quantum computation. In this work, we provide the first complete characterization of these sources of error in a neutral-atom quantum computer and propose hardware-efficient, fault-tolerant quantum computation schemes that mitigate them. Notably, we develop a novel and distinctly efficient method to address the most important errors associated with the decay of atomic qubits to states outside of the computational subspace. These advances allow us to significantly reduce the resource cost for fault-tolerant quantum computation compared to existing, general-purpose schemes. Our protocols can be implemented in the near term using state-of-the-art neutral-atom platforms with qubits encoded in both alkali and alkaline-earth atoms.
Alzheimer's disease (AD) pathogenesis is widely believed to be driven by the production and deposition of the amyloid-beta peptide (Abeta). For many years, investigators have been puzzled by the weak ...to nonexistent correlation between the amount of neuritic plaque pathology in the human brain and the degree of clinical dementia. Recent advances in our understanding of the development of amyloid pathology have helped solve this mystery. Substantial evidence now indicates that the solubility of Abeta, and the quantity of Abeta in different pools, may be more closely related to disease state. The composition of these pools of Abeta reflects different populations of amyloid deposits and has definite correlates with the clinical status of the patient. Imaging technologies, including new amyloid imaging agents based on the chemical structure of histologic dyes, are now making it possible to track amyloid pathology along with disease progression in the living patient. Interestingly, these approaches indicate that the Abeta deposited in AD is different from that found in animal models. In general, deposited Abeta is more easily cleared from the brain in animal models and does not show the same physical and biochemical characteristics as the amyloid found in AD. This raises important issues regarding the development and testing of future therapeutic agents.
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