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All-solid-state batteries (ASSBs) with Li metal anodes or Si anodes are promising candidates to achieve high energy density and improved safety, but they suffer from undesirable lithium dendrite growth or huge volume expansion, respectively. Here we synthesize a hard-carbon-stabilized Li–Si alloy anode in which sintering of Si leads to the transformation of micro-metre particles into dense continuum. A 3D ionic-electronic-conductive network composed of plastically deformable Li-rich phases (Li 15 Si 4 and LiC 6 ) that enlarges active area and relieves stress concentration is created in the anode, leading to improved electrode kinetics and mechanical stability. With the hard-carbon-stabilized Li-Si anode, full cells using LiCoO 2 or LiNi 0.8 Co 0.1 Mn 0.1 O 2 cathodes and Li 6 PS 5 Cl electrolyte achieve favourable rate capability and cycle stability. In particular, the ASSB with LiNi 0.8 Co 0.1 Mn 0.1 O 2 at high loading of 5.86 mAh cm −2 delivers 5,000 cycles at 1 C (5.86 mA cm −2 ), demonstrating the potential of using hard-carbon-stabilized Li–Si alloy anodes for practical applications of ASSBs. Si anodes could be an alternative to Li anodes in the application of solid-state batteries, but they suffer from issues such as severe volume expansion and sluggish kinetics. Here the researchers develop a Li–Si alloy anode that is stabilized by hard carbon, which leads to exceptional high-performance solid-state batteries.

Introduction Traumatic brain injury (TBI) is considered as the most robust environmental risk factor for Alzheimer’s disease (AD). Besides direct neuronal injury and neuroinflammation, vascular impairment is also a hallmark event of the pathological cascade after TBI. However, the vascular connection between TBI and subsequent AD pathogenesis remains underexplored. Methods In a closed-head mild TBI (mTBI) model in mice with controlled cortical impact, we examined the time courses of microvascular injury, blood–brain barrier (BBB) dysfunction, gliosis and motor function impairment in wild type C57BL/6 mice. We also evaluated the BBB integrity, amyloid pathology as well as cognitive functions after mTBI in the 5xFAD mouse model of AD. Results mTBI induced microvascular injury with BBB breakdown, pericyte loss, basement membrane alteration and cerebral blood flow reduction in mice, in which BBB breakdown preceded gliosis. More importantly, mTBI accelerated BBB leakage, amyloid pathology and cognitive impairment in the 5xFAD mice. Discussion Our data demonstrated that microvascular injury plays a key role in the pathogenesis of AD after mTBI. Therefore, restoring vascular functions might be beneficial for patients with mTBI, and potentially reduce the risk of developing AD.