Yongjun Jiang

[This corrects the article DOI: 10.3389/fnins.2022.1086168.].

Background: As a well‐recognized vascular variation, hypoplastic vertebral artery has been recognized as a potential risk for stroke. We aimed to assess the odds of new‐onset stroke over a 20‐year period in subjects with versus without hypoplastic vertebral artery, exploring how the progression of basilar artery bending mediates the odds. Methods: This was a retrospective cohort study, with 20 years of follow‐up (2004–2024, analysis performed in June 2025). The primary outcome was the occurrence of new‐onset posterior circulation infarction during follow‐up. Logistic regression models were fitted for new‐onset posterior circulation infarction as gender, baseline stroke, baseline posterior circulation infarction, basilar artery stenosis during follow‐up, the progression of basilar artery bending, and hypoplastic vertebral artery. Mediation analyses were conducted for vertebral artery stenosis during follow‐up, basilar artery stenosis during follow‐up, and the progression of basilar artery bending. Results: A total of 1464 subjects were included, 547 with hypoplastic vertebral artery. During the 20‐year follow‐up, 91 participants had new‐onset posterior circulation infarction. The occurrence of new‐onset posterior circulation infarction was significantly associated with progression of basilar artery bending (odds ratio 1.700, 95% confidence interval 1.032–2.798, p  = 0.037) and hypoplastic vertebral artery (odds ratio 1.481, 95% confidence interval 1.019–2.003, p  = 0.015). The proportion of new‐onset posterior circulation infarction attributable to hypoplastic vertebral artery was mediated by the progression of basilar artery bending, accounting for approximately 50.2% (95% confidence interval 3.2%–102.4%). Conclusions: Results of this study revealed that hypoplastic vertebral artery was associated with new‐onset posterior circulation infarction, and progression of basilar artery bending may serve as a potential intermediate factor in this association.

Atherosclerosis is characterized by chronic low-grade inflammation (LGI) of the arteries. An elevated LGI score has been associated with the onset and recurrence of cardio-cerebrovascular diseases. The aim of this multicenter hospital-based prospective cohort study was to investigate the relationship between the LGI score and stroke recurrence in patients with intracranial atherosclerotic stenosis (ICAS).Consecutive acute ischemic stroke patients admitted within 1 week after onset were screened. The intracranial arteries were evaluated via computed tomographic angiography, magnetic resonance angiography or digital subtraction angiography. Patients with ICAS were enrolled and followed up for at least 1 year. The primary outcome was ischemic stroke recurrence. Cox regression and Kaplan‒Meier survival curves were used to analyze the association of the LGI score and stroke recurrence. A total of 932 patients were divided into 4 groups according to the LGI quartiles (Q1: < 3; Q2: 3–7; Q3: 7–10; Q4: > 10). At the end of follow-up (37.37 ± 15.24 months), 80 patients experienced at least one recurrent ischemic stroke. There were significant differences in total cholesterol levels, C-reactive protein levels, white blood cell counts, platelet counts, neutrophil-to-lymphocyte ratios, and stroke recurrence among the 4 groups. According to the multivariate adjusted models, compared to that for Q1, the hazard ratio for stroke recurrence in patients in Q4 was 2.748 (1.303–5.797). The Kaplan–Meier survival (ischemic stroke-free) curves according to quartiles of the LGI score also showed significant differences (log-rank test, P = 0.016). Our findings suggested that the LGI score was an independent risk factor for ischemic stroke recurrence in patients with ICAS.

Background Symptomatic intracranial atherosclerotic stenosis (ICAS) is prone to cause early recurrent stroke (ERS). Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors lower low-density lipoprotein cholesterol (LDL-C) levels and prevent cardiovascular events. This multicentre, hospital-based prospective cohort study was designed to investigate whether PCSK9 inhibitors would prevent ERS in patients with symptomatic ICAS. Methods From 1 October 2020 to 30 September 2022, consecutive patients with acute ischaemic stroke attributed to ICAS admitted within 1 week after onset were enrolled and followed up for 1 month. Patients were divided into two groups, the PCSK9 inhibitors group receiving PCSK9 inhibitors add-on therapy, and the control group receiving statins and/or ezetimibe. The primary outcome was ERS. Cox proportional hazard models and Kaplan-Meier survival curve were used to estimate the association between PCSK9 inhibitors and ERS. Results At the end of follow-up, the LDL-C levels were further lowered by PCSK9 inhibitors add-on therapy (n=232, from 3.06±1.16 mmol/L to 2.12±1.19 mmol/L) than statins and/or ezetimibe treatment (n=429, from 2.91±1.05 mmol/L to 2.64±0.86 mmol/L, pConclusions In our study, PCSK9 inhibitors add-on therapy further reduced LDL-C levels and ERS in patients with symptomatic ICAS.

Background: Brainstem stroke causes severe and persistent neurological impairment. Due to the limited spontaneous recovery and regeneration of the disrupted neural circuits, transplantation of exogenous neural stem cells (NSCs) was an alternative, while there were limitations for primitive NSCs. Methods: We established a mouse model of brainstem stroke by injecting endothelin in the right pons. Brain-derived neurotrophic factor (BDNF)- and distal-less homeobox 2 (Dlx2)-modified NSCs were transplanted to treat brainstem stroke. Transsynaptic viral tracking, immunostaining, magnetic resonance imaging, behavioral testing, and whole-cell patch clamp recordings were applied to probe the pathophysiology and therapeutic prospects of BDNF- and Dlx2-modified NSCs. Results: GABAergic neurons were predominantly lost after the brainstem stroke. No endogenous NSCs were generated in situ or migrated from the neurogenesis niches within the brainstem infarct region. Co-overexpressions of BDNF and Dlx2 not only promoted the survival of NSCs, but also boosted the differentiation of NSCs into GABAergic neurons. Results from transsynaptic virus tracking, immunostaining, and evidence from whole-cell patch clamping revealed the morphological and functional integration of the grafted BDNF- and Dlx2-modified NSCs-derived neurons with the host neural circuits. Neurological function was improved by transplantation of BDNF- and Dlx2-modified NSCs in brainstem stroke. Conclusions: These findings demonstrated that BDNF- and Dlx2-modified NSCs differentiated into GABAergic neurons, integrated into and reconstituted the host neural networks, and alleviated the ischemic injury. It thus provided a potential therapeutic strategy for brainstem stroke.

Editorial: the role of diabetes in the pathophysiology and prognosis of ischemic stroke

Background and Purpose: Hyperglycemia has been associated with unfavorable outcome of acute ischemic stroke, but this association has not been verified in patients with endovascular thrombectomy treatment. This study aimed to assess the impact of stress hyperglycemia ratio on early neurological deterioration and favorable outcome after thrombectomy in patients with acute ischemic stroke.Methods: Stroke patients with endovascular thrombectomy in two comprehensive centers were enrolled. Early neurological deterioration was defined as ≥4 points increase of National Institutes of Health Stroke Scale (NIHSS) at 24 hours after endovascular procedure. Favorable outcome was defined as modified Rankin Scale (mRS) score of 0-2 at 90 days of stroke onset. Multivariate regression analysis was used to identify the predictors for early neurological deterioration and favorable outcome.Results: Among the 559 enrolled, 74 (13.2%) patients developed early neurological deterioration. The predictors for early neurological deterioration were high stress hyperglycemia ratio at baseline (OR =5.77; 95% CI, 1.878-17.742; P =0.002), symptomatic intracranial hemorrhage (OR =4.90; 95% CI, 2.439-9.835; P <0.001) and high NIHSS score after 24 hours (OR =1.11; 95% CI, 1.071-1.151; P <0.001). The predictors for favorable outcome were stress hyperglycemia ratio (OR =0.196, 95% CI, 0.077-0.502; P =0.001), age (OR =0.942, 95% CI, 0.909-0.977; P =0.001), NIHSS score 24 hours after onset (OR =0.757, 95% CI =0.693-0.827; P P =0.025), poor collateral status before treatment (ASITN/SIR grade 0-3, OR =62.017, 95% CI, 25.920-148.382; P <0.001), successful recanalization (mTICI 2b or 3, OR =7.415, 95% CI, 1.942-28.313; P =0.001).Conclusion: High stress hyperglycemia ratio may be related to early neurological deterioration and decreased likelihood of favourable outcomes after endovascular thrombectomy in patients with acute ischemic stroke.