Albumin is the most abundant protein in plasma and is synthesized primarily in the liver. It has a variety of biological roles, such as increasing colloid osmotic pressure, and performing antioxidant, anti-inflammatory, and substance transportation functions. Several studies have confirmed that albumin has neuroprotective effects and it has been used in the treatment of cerebral edema and increased intracranial pressure. In this review we focus on the neuroprotective effects of albumin in ischemic stroke, such as the reduction of cerebral edema, antioxidant effects, protection of neuronal cell membranes, and increased cerebral blood flow. In addition, we summarize preclinical and clinical studies of albumin in ischemic stroke. We believe that the neuroprotective role of albumin should be re-investigated in the era of reperfusion therapy.

Venous sinus stent implantation is an emerging endovascular treatment technique effectively applied in diseases such as cerebral venous sinus thrombosis. However, arterial stents are commonly used in clinical practice for venous sinus stent implantation, which is off-label and carries high risks and poor prognosis, highlighting the necessity of developing venous sinus-specific stents. This narrative review discusses the current situation and problems of venous sinus stent implantation and looks forward to the design focus and future development prospects of venous sinus-specific stents.

This review discusses the roles of brain-derived neurotrophic factor (BDNF) and precursor BDNF (proBDNF) in schizophrenia (SCZ). SCZ is associated with neuronal dysfunction, altered synaptic plasticity, and cognitive deficits. BDNF positively promotes neuronal growth, differentiation, and synapse formation, and regulates synaptic transmission and plasticity. ProBDNF negatively affects neuronal survival and synaptic remodeling, however, by binding to its neurotrophin receptor p75 (p75NTR). A better understanding of the pathogenesis of SCZ vis-à-vis BDNF and proBDNF may provide new directions and strategies for its treatment.

Objective: To investigate clinical significance of the effects of smoking on blood lipids, C-reactive protein, and homocysteine in young ischemic stroke patients. Methods: The clinical data of 423 young stroke patients in the department of neurology at Taihe Hospital in Shiyan City, China were retrospectively analyzed, including age, gender, drinking history, family history, and atrial fibrillation history. Patients were divided into two groups according to whether they smoked, and the blood lipids, C-reactive protein, and homocysteine were compared between groups. Results: The proportion of smokers was 41.83%. The levels of total cholesterol, triglycerides (TG), low density lipoprotein (LDL), and homocysteine were higher in patients who smoked than in those who did not (P＜0.05). High density lipoprotein (HDL) was lower in the smoking group (P＜0.05). C-reactive protein test results were divided into groups according to whether the levels exceeded the normal range or not, and no correlation was found between C-reactive protein levels and smoking (P＞0.05). Conclusion: Total cholesterol, TG, LDL, HDL, and homocysteine were significantly different between stroke patients who smoked and those who did not. We therefore suggest that smoking cessation take place as soon as possible and that it be avoided entirely in order to reduce the incidence of atherosclerosis and stroke.

Myelopathy is a common etiology of acute bilateral limb weakness. While painless acute aortic dissection (AAD) is the most common catastrophic event that can mimic myelopathic manifestations of acute bilateral limb weakness, it is often easily ignoredWe describe a case of painless AAD in a 70-year-old man with a history of hypertension manifesting as acute myelopathy (bilateral limb weakness and loss of all types of sensation) with increased levels of serum myoglobin and D-dimer. Magnetic resonance imaging of the spinal cord revealed a normal thoracic and lumbar spinal cord but a dissection of the thoracic aorta. Computed tomography angiography of the chest and abdominal aorta showed a Stanford type B dissection extending throughout the thoracic aorta and into the abdominal aorta hypomere. The patient died because of a sudden drop in blood pressure during transfer to vascular surgery. The clinical presentation of painless AAD mimics myelopathies. Aortic dissection should be considered in patients presenting with acute bilateral limb weakness. Physical examination of the skin temperature, dorsalis pedis artery, serum D-dimer, and myocardial markers can provide diagnostic clues.