Cognitive impairment includes several clinical processes from mild cognitive impairment to dementia, and now it has been a serious public health problem, as there is no effective treatment, it has caused a heavy economic and psychological burden on the family and society, therefore, it seems important to find effective intervention means.Vitamin D is an essential nutrient element for the human body, more and more evidences show that it also participates in many extraskeletal biological reactions, such as nervous system regulatory processes, in addition to calcium and phosphorus metabolism.Several researches have revealed that Vitamin D deficiency is associated with impaired cognition, the mechanisms mediating this link are poorly understood, what's more, for further clinical application, we need to solve the problems like choosing the suitable populations and drug dosage, therefore, this article summarizes and analyzes the effects of serum Vitamin D levels on the cognitive function of different populations, the research progress of Vitamin D intervention research and its possible mechanism of action, hoping to provide references for the clinical application of Vitamin D in the treatment of cognitive impairment.The results show that Vitamin D deficiency is related to the decline of cognitive function in different populations, and Vitamin D can improve cognitive function through reducing Aβ toxicity, anti-inflammatory and anti-oxidative stress and other mechanisms, its supplementation is expected to be an important measure of treating cognitive impairment, in the future, large-scale longitudinal cohort studies are needed to determine the optimal dosage and duration of treatment.

Vascular cognitive impairment (VCI) is a progressive cognitive impairment caused by cerebrovascular disease or vascular risk factors. It is the second common type of cognitive impairment after Alzheimer's disease. VCI can be caused by a variety of signal and metabolic pathways. Its core mechanism is that cerebrovascular disease destroys the neurovascular unit composed of neurons, glial cells, and cerebrovascular endothelial cells. This article summarizes and discusses the known mechanisms of VCI, in order to deepen the understanding of the molecular pathological process of VCI and provide ideas for its prevention and treatment.

Objective:To investigate the factors associated with delay in anticoagulant therapy in patients with cerebral venous sinus thrombosis (CVST) and its effect on outcome.Methods:Patients with CVST admitted to Changhai Hospital, Naval Medical University from January 2010 to August 2021 were retrospectively enrolled. Patients were divided into early anticoagulation group and late anticoagulation group by the median time interval from first symptom to initiation of anticoagulation. The modified Rankin Scale was used for outcome assessment at 90 d after onset. 0-2 scores were defined as good outcome and 3-6 were defined as poor outcome. Demographic and clinical data were compared for the early versus late anticoagulation group and for the good versus poor outcome groups. Multivariable logistic regression was used to identify independent influencing factors of delay in anticoagulation and the correlation of delay in anticoagulation with poor outcome. Results:A total of 131 patients were included, their age was 40.07±15.11 years old, and 68 (51.91%) were male. Of these, 65 patients (49.62%) were in the early anticoagulation group and 14 (10.69%) were in the poor outcome group. Compared with the late anticoagulation group, the early anticoagulation group had a significantly higher proportion of patients with seizures and brain parenchymal damage as well as higher D-dimer levels on admission, while the proportion of patients with visual impairment/papilloedema was significantly lower (all P<0.05). Compared with the good outcome group, the poor outcome group had significantly higher proportions of patients with seizures, dyskinesia, impaired consciousness, low Glasgow Coma Scale score, and brain parenchymal damage as well as higher D-dimer, total cholesterol and low density lipoprotein cholesterol levels, sites of thrombus involvement were more common in the superior sagittal and straight sinuses, and significantly lower proportions of patients with headache and lower albumin levels on admission (all P<0.05). Multivariate logistic regression analysis showed that visual impairment/papilloedema (odds ratio [ OR] 0.119, 95% confidence interval [ CI] 0.030-0.473; P=0.002) and brain parenchymal damage ( OR 1.341, 95% CI 1.042-1.727; P=0.023) were independently associated with a delay in anticoagulation treatment, and a delay in anticoagulation treatment ( OR 6.102, 95% CI 1.185-30.504; P=0.030) and D-dimer level on admission ( OR 1.299, 95% CI 1.141-1.480; P<0.001) were the independent predictors of poor outcome in patients with CVST. Conclusions:Visual impairment/papilloedema and absence of brain parenchymal damage on cranial imaging are the independent risk factors for delay in anticoagulation in patients with CVST. The delay in anticoagulation is strongly associated with the poor outcome in patients with CVST.