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Commercial lithium-ion batteries that use flammable liquid electrolytes face significant safety risks, such as fires caused by electrolyte leaks. Solid polymer electrolytes (SPEs) present a viable solution to this problem, with ether-based polymer electrolytes standing out due to their superior stability and compatibility with lithium metal. The in situ ring-opening polymerization of cyclic ether monomers not only simplifies the battery manufacturing process but also improves the solid/solid interfacial contacts between electrolytes and electrodes, thereby significantly reducing interfacial impedance. In this paper, we review the mechanisms of ring-opening polymerization for cyclic ether monomers and analyze the ionic conduction of ether-based polymer electrolytes. We also explore the in situ curing mechanisms for several representative cyclic ether monomers and assess research advancements in this area. Additionally, this paper discusses the sustainability of ether-based polymer electrolytes and provides an outlook on future research and sustainability initiatives in the field.

Introduction: Vascular cognitive impairment (VCI) is highly heterogeneous, with unclear pathogenesis. Individuals with vascular risk factors (VRF), cerebral small vessel disease (CSVD), and stroke are all at risk of developing VCI. To address the growing challenges posed by VCI, the "Vascular, Imaging and Cognition Association of China" (VICA) was established., Methods: VICA aims to recruit 10,000 participants, including 2000 with VRF, 3000 with CSVD, and 5000 stroke patients, to form a nationwide multicenter cohort. The study integrates clinical, neuroimaging, and multi-omics data to better understand VCI heterogeneity, improve disease prediction, and ensure timely diagnosis., Results: VICA has screened 2045 eligible VRF participants from six communities in Wuhan, Shanghai, and Taizhou, along with 602 CSVD and 1269 stroke patients from 135 hospitals nationwide. Baseline enrollment and follow-up work are still ongoing., Discussion: Establishing a high-quality longitudinal cohort is crucial for understanding VCI pathogenesis and developing novel markers for early screening and diagnosis., Highlights: Establish a large-scale prospective longitudinal cohort comprising 10,000 participants, focusing on the high-risk population of vascular cognitive impairment (VCI) in China. Establish a nationwide three-tier medical network, make full use of resources, and achieve extensive enrollment of patients with cerebral small vessel disease and stroke patients. Utilize multimodal imaging and biomarkers to lay the foundation for constructing more-precise risk models. Introduce eye movement and gait analysis as new methods for assessing cognitive function. Use positron emission tomography to further investigate the interaction between vascular factors and neurodegeneration., (© 2024 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)

Progressive neuronal loss is a hallmark feature distinguishing neurodegenerative diseases from normal ageing. However, the underlying mechanisms remain unknown. Extracellular K+ homeostasis is a potential mediator of neuronal injury as K+ elevations increase excitatory activity. The dysregulation of extracellular K+ and potassium channel expressions during neurodegeneration could contribute to this distinction. Here we measured the cortical extracellular K+ concentration ([K+]e) in awake wild-type mice as well as murine models of neurodegeneration using K+-sensitive microelectrodes. Unexpectedly, aged wild-type mice exhibited significantly lower cortical [K+]e than young mice. In contrast, cortical [K+]e was consistently elevated in Alzheimer's disease (APP/PS1), amyotrophic lateral sclerosis (ALS) (SOD1G93A) and Huntington's disease (R6/2) models. Cortical resting [K+]e correlated inversely with neuronal density and the [K+]e buffering rate but correlated positively with the predicted neuronal firing rate. Screening of astrocyte-selective genomic datasets revealed a number of potassium channel genes that were downregulated in these disease models but not in normal ageing. In particular, the inwardly rectifying potassium channel Kcnj10 was downregulated in ALS and Huntington's disease models but not in normal ageing, while Fxyd1 and Slc1a3, each of which acts as a negative regulator of potassium uptake, were each upregulated by astrocytes in both Alzheimer's disease and ALS models. Chronic elevation of [K+]e in response to changes in gene expression and the attendant neuronal hyperexcitability may drive the neuronal loss characteristic of these neurodegenerative diseases. These observations suggest that the dysregulation of extracellular K+ homeostasis in a number of neurodegenerative diseases could be due to aberrant astrocytic K+ buffering and as such, highlight a fundamental role for glial dysfunction in neurodegeneration., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)