Stroke最新文献

Delays in stroke diagnosis contribute to long-term disability. Many patients still face barriers to effective risk factor management, timely detection, and access to poststroke rehabilitation. The emergence of artificial intelligence-enabled, consumer-facing health technologies offers a transformative opportunity to address these gaps across the stroke care continuum. This review examines the evolving role of artificial intelligence-powered devices, including smartwatches, smartphones, wearable sensors, and ambient home-based technologies, in enabling precision stroke care. For stroke prevention, these tools facilitate scalable monitoring of cardiometabolic and stroke-specific risk factors. For early detection, artificial intelligence algorithms applied to multimodal sensor data can identify subtle neurological impairments and support real-time triage. In recovery, artificial intelligence-enhanced remote monitoring and virtual supervision offer scalable models for delivering personalized rehabilitation outside of specialized centers. Although most of these innovations remain in early development, they signal a paradigm shift toward accessible, individualized, and data-driven stroke prevention and management.

HIV-associated comorbidities, including cardiovascular and cerebrovascular events, are frequent diseases in people living with HIV. Notably, the prevalence of ischemic stroke is 3× higher in people living with HIV than in noninfected individuals, making it one of the most significant cerebrovascular events in people living with HIV. Despite this close association, the mechanisms involved in the enhanced incidence of ischemic stroke in HIV infection remain poorly understood. A chemokine CCL2 (C-C motif chemokine ligand 2), acting via its receptor CCR2 (C-C chemokine receptor type 2), is a prominent chemoattractant involved in the recruitment of CD4+T cells and monocytes/macrophages, which are primary targets for HIV infection. Due to its role in directing leukocyte migration into the brain and enhancing blood-brain barrier permeability, CCL2 is also a critical mediator of neuroinflammation after brain damage, such as ischemic stroke. In this review, we examine the role of the CCL2/CCR2 signaling pathway in HIV infection, its influence on the progression of ischemic stroke outcome and recovery, and propose the CCL2/CCR2 axis as a possible therapeutic target in people living with HIV.

Background: The health outcomes currently reported in aneurysmal subarachnoid hemorrhage (aSAH) research lack consistency and do not sufficiently reflect what is important to people most affected. The objective of this article was to establish consensus on the aspects of health (domains) clinicians and researchers should measure in aSAH research.

Methods: Informed by 2 international prioritizing surveys (involving 239 participants from over 25 countries and 6 continents), we used established consensus methodology in a hybrid in-person/online consensus meeting to establish which domains of health researchers should measure in aSAH research. Sixty-nine participants with lived experience with aSAH (35%), clinical and research leaders (62%), or from aSAH-related charity (3%) took part. International multidisciplinary working groups established consensus definitions for each domain.

Results: Consensus (>70% endorsement) was sought on a proposed group of 6 domains of health, and failing that, each domain individually. The 6 domains which reached consensus and were formally defined are (1) health-related quality of life, (2) survival, (3) cognition and executive function, (4) functional outcome, (5) delayed cerebral ischemia and cerebral infarction, and (6) rebleeding and aneurysm obliteration.

Conclusions: This International Position Statement reports the consensus process undertaken and the core domain set established to guide the choice of outcomes for evaluating new treatments for aSAH. It will ultimately help shape the future aSAH research agenda.

Background: Vascular cognitive impairment (VCI) is a cognitive decline attributed to vascular pathology. Human peripheral blood mononuclear cells (PBMCs) are the key drivers of immune and inflammatory responses in circulation and are thought to play an important role in VCI, but the mechanism is unclear. The nicotinamide adenine dinucleotide (NAD⁺) salvage pathway uses NAD⁺ breakdown products to synthesize new NAD⁺ and maintain its cellular levels. Dysregulation of this pathway may disrupt cellular metabolism and immune balance, contributing to disease. Here, we investigated whether peripheral inflammation triggered by PBMCs is linked to the aberrant NAD⁺ metabolism that occurs in VCI. Targeting the NAD⁺ salvage pathway was also explored as a potential therapeutic strategy for VCI.

Methods: PBMCs from patients with VCI or controls were subjected to RNA sequencing and cultured with autologous serum. The levels of proinflammatory cytokines in PBMCs and key components in the NAD⁺ salvage pathway were measured. These parameters were assessed in a VCI mouse model. The 5'-Phosphoribosyl-pyrophosphate (PRPP), a critical substrate for NAD⁺ salvage biosynthesis, was administered, and its therapeutic effects on cognitive function were evaluated.

Results: Peripheral PBMCs from VCI patients showed elevated proinflammatory cytokine levels, reduced iNAMPT (intracellular nicotinamide phosphoribosyltransferase) activity, and lower NAD⁺ levels, whereas eNAMPT (extracellular NAMPT) levels were significantly higher. Pharmacological inhibition of eNAMPT with FK866 reduced inflammation in VCI PBMCs. Additionally, blocking TLR4 or CCR5 alleviated the proinflammatory response triggered by eNAMPT. In the VCI mice model, the NAD⁺ salvage pathway was impaired in PBMCs, which exhibited proinflammatory activity. 5'-phosphoribosyl-pyrophosphate administration restored NAD⁺ levels, suppressed inflammation, and improved cognitive function.

Conclusions: Our findings suggest peripheral inflammation driven by impaired NAD⁺ salvage and elevated eNAMPT levels in PBMCs plays a key role in VCI pathogenesis. Restoring NAD⁺ homeostasis via 5'-phosphoribosyl-pyrophosphate treatment significantly improved cognition in VCI mice, highlighting NAD⁺ salvage as a potential therapeutic target.