Enriched environment priors to TET1 hippocampal administration for regulating psychiatric behaviors via glial reactivity in chronic cerebral hypoperfusion models.

Background: Chronic cerebral hypoperfusion (CCH) has been gradually regarded as a common etiologic mechanism for cognitive and psychiatric disturbances. Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) played an important role in adult hippocampal neurogenesis (AHN), neuronal circuits formation, cognition and psychiatric disorders. Enriched environment (EE) showed a beneficial effect on cognition and depression via effectively regulating AHN and glial reactivity.

Dimethyl fumarate improves cognitive deficits in chronic cerebral hypoperfusion rats by alleviating inflammation, oxidative stress, and ferroptosis via NRF2/ARE/NF-κB signal pathway.

Cerebrovascular disease and its risk factors cause persistent decrease of cerebral blood flow, chronic cerebral hypoperfusion (CCH) is the major foundation of vascular cognitive impairment (VCI). The hippocampus is extremely vulnerable to cerebral ischemia and hypoxia. Oxidative stress and neuroinflammation injury are important pathophysiological mechanisms of this process, which is closely related to hippocampal neurons damage and loss.

A simple-to-use web-based calculator for survival prediction in Parkinson's disease.

Background: To establish and validate a nomogram and corresponding web-based calculator to predict the survival of patients with Parkinson's disease (PD).

Methods: In this cohort study, we retrospectively evaluated patients (n=497) with PD using a two-stage design, from March 2004 to November 2007 and from July 2005 to July 2015. Predictive variables included in the model were identified by univariate and multiple Cox proportional hazard analyses in the training set.

Neurological Implications of Non-critically Ill Patients With Coronavirus Disease 2019 in a Fangcang Shelter Hospital in Wuhan, China.

Coronavirus disease 2019 (COVID-19) is a new viral respiratory disease and has become a pandemic. Fever, weakness, and dry cough are the main clinical manifestations. However, little is known about neurological symptoms of non-critically ill COVID-19 patients.

Medium Term Follow-Up of 337 Patients With Coronavirus Disease 2019 (COVID-19) in a Fangcang Shelter Hospital in Wuhan, China.

With the adoption of powerful preventive and therapeutic measures, a large number of patients with COVID-19 have recovered and been discharged from hospitals in Wuhan, China. Prevention of epidemic rebound is a top priority of current works. However, information regarding post-discharge quarantine and surveillance of recovered patients with COVID-19 is scarce.

Iron Metabolism, Ferroptosis, and the Links With Alzheimer's Disease.

Iron is an essential transition metal for numerous biologic processes in mammals. Iron metabolism is regulated via several coordination mechanisms including absorption, utilization, recycling, and storage. Iron dyshomeostasis can result in intracellular iron retention, thereby damaging cells, tissues, and organs through free oxygen radical generation.

The Emerging Roles of Ferroptosis in Vascular Cognitive Impairment.

Vascular cognitive impairment (VCI) is a clinical syndrome that encompasses all forms of cognitive deficits caused by cerebrovascular disease, from mild cognitive impairment to dementia. Vascular dementia, the second most common type of dementia after Alzheimer's disease (AD), accounts for approximately 20% of dementia patients. Ferroptosis is a recently defined iron-dependent form of cell death, which is distinct from apoptosis, necrosis, autophagy, and other forms of cell death.

Promotion of anoxia-reoxygenation-induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase-activated MAPK signaling in human umbilical vein endothelial cells.

Previous studies have demonstrated that nicotinamide phosphoribosyltransferase (NAMPT) promoted inflammation and permeability of vascular endothelial cells following cardiopulmonary bypass (CPB). In addition, mitogen-activated protein kinase (MAPK) signaling was activated and contributed to these cell responses. However, the mechanism by which NAMPT regulates cellular inflammation and permeability remains unknown, and whether NAMPT regulates MAPK signaling during this process is also not clear.