Impact of the COVID-19 pandemic on acute stroke care: An analysis of the 24-month data from a comprehensive stroke center in Shanghai, China.

Introduction: Whether the coronavirus disease-2019 (COVID-19) pandemic is associated with a long-term negative impact on acute stroke care remains uncertain. This study aims to compare the timing of key aspects of stroke codes between patients before and after the COVID-19 pandemic.

Methods: This retrospective cohort study was conducted at an academic hospital in Shanghai, China and included all adult patients with acute ischemic stroke hospitalized via the emergency department (ED) stroke pathway during the 24 months since the COVID-19 outbreak (COVID-19: January 1, 2020-December 31, 2021).

Blood BMP6 Associated with Cognitive Performance and Alzheimer's Disease Diagnosis: A Longitudinal Study of Elders.

Background: Bone morphogenetic protein (BMP) plays important roles in the pathology of Alzheimer's disease (AD).

Objective: We sought blood BMP6 involved in the processes underlying cognitive decline and detected them in association with AD.

Methods: A total of 309 participants in Shanghai Mental Health Center (SMHC) and 547 participants in Alzheimer's disease Neuroimaging Initiative (ADNI) cohort were included.

Using a new HSPC senescence model in vitro to explore the mechanism of cellular memory in aging HSPCs.

Background: Age-associated changes attenuate human blood system functionality through the aging of hematopoietic stem and progenitor cells (HSPCs), manifested in human populations an increase in myeloproliferative disease and even leukemia; therefore, study on HSPC senescence bears great significance to treat hematopoietic-associated disease. Furthermore, the mechanism of HSPC aging is lacking, especially the cellular memory mechanism. Here, we not only reported a new HSPC senescence model in vitro, but also propose and verify the cellular memory mechanism of HSPC aging of the Polycomb/Trithorax system.

Targeted disruption of supraspinal motor circuitry reveals a distributed network underlying Restless Legs Syndrome (RLS)-like movements in the rat.

In this study we uncovered, through targeted ablation, a potential role for corticospinal, cerebello-rubro-spinal, and hypothalamic A11 dopaminergic systems in the development of restless legs syndrome (RLS)-like movements during sleep. Targeted lesions in select basal ganglia (BG) structures also revealed a major role for nigrostriatal dopamine, the striatum, and the external globus pallidus (GPe) in regulating RLS-like movements, in particular pallidocortical projections from the GPe to the motor cortex. We further showed that pramipexiole, a dopamine agonist used to treat human RLS, reduced RLS-like movements.

Ventral medullary control of rapid eye movement sleep and atonia.

Discrete populations of neurons at multiple levels of the brainstem control rapid eye movement (REM) sleep and the accompanying loss of postural muscle tone, or atonia. The specific contributions of these brainstem cell populations to REM sleep control remains incompletely understood. Here we show in rats that viral vector-based lesions of the ventromedial medulla at a level rostral to the inferior olive (pSOM) produced violent myoclonic twitches and abnormal electromyographic spikes, but not complete loss of tonic atonia, during REM sleep.

Movement deficits and neuronal loss in basal ganglia in TRPC1 deficient mice.

Transient receptor potential cation (TRPC) channel proteins are abundantly expressed in brain. However, the functions of these TRPC proteins such as TRPC1 are largely unclear. In this study, we reported that TRPC1 deficiency caused movement disorder as measured by swimming test, modified open field test and sunflower seeds eating test.

Increased apoptosis in the platelets of patients with Alzheimer's disease and amnestic mild cognitive impairment.

Objectives: Alzheimer's disease (AD), the most common cause of dementia, is a progressive, incurable neurodegenerative disorder. Platelet is a suitable source of human peripheral tissue to study pathological mechanisms occurring in the brain. The present study aims to investigate (1) whether abnormal apoptotic events besides involved in AD within the central neurologic system, could also occur at peripheral platelet level; (2) whether apoptosis at peripheral platelet level starts at the early stage of AD.

LIMK1 is involved in the protective effects of bone morphogenetic protein 6 against amyloid-β-induced neurotoxicity in rat hippocampal neurons.

Bone morphogenetic protein 6 (BMP6) has neuroprotective effects against various neuronal injuries, but its effect on amyloid-β (Aβ)-induced neurotoxicity remains unclear. We exposed rat hippocampal neurons to different concentrations of Aβ25-35 to induce neurotoxicity, and then treated cells with BMP6 to assess the neuroprotective effects. In vivo, we bilaterally injected Aβ1-40 into basal forebrain to simulate the neuropathological process of Alzheimer's disease (AD), and explored changes in the expression of BMP6 and LIMK1.

A 14-year-old girl with an unusual combination of incontinentia pigmenti and conversion disorder.

Incontinentia pigmenti is a rare X-linked neurological-skin genetic disease. Some studies have shown that about 30~40% of patients with IP have varying symptoms of eye/central nervous system which are the major causes of disability. Conversion disorder is one of the most common mental diseases in children and may exhibit the single or multiple neurological symptoms.

Serum levels of inflammation factors and cognitive performance in amnestic mild cognitive impairment: a Chinese clinical study.

Early diagnosis of Alzheimer's disease (AD) is important for initiating timely therapy to block or slow the rate of disease progression. This study was designed to investigate the potential of inflammation-related biomarkers in peripheral blood to accurately reflect AD onset and progression. Individuals (n=150) with amnestic mild cognitive impairment (aMCI) were divided into two subgroups (low- and high-risk) based on APOEε4 allele carrier status, and administered a battery of neuropsychological tests and tested for serum levels of IL-6, IL-10, TNF-α, and IFN-γ by using specific enzyme-linked immunosorbent assays.

A clinical memory battery for screening for amnestic mild cognitive impairment in an elderly chinese population.

Amnestic mild cognitive impairment (MCI) might be more likely to progress to Alzheimer's disease than single non-memory MCI and multiple domain MCI. After excluding those who did not conform to the inclusion criteria of amnestic MCI or healthy controls, a neuropsychologic battery that included the Mini-Mental State Examination, Clinical Dementia Rating, Chinese version of the Montreal Cognitive Assessment, Instrumental Activities of Daily Living scale and Auditory Verbal Learning Test was performed on 150 amnestic MCI and 150 normal control patients. The Chinese version of the Montreal Cognitive Assessment was measured for its test-retest reliability, sensitivity and specificity.

Involvement of IRE1α signaling in the hippocampus in patients with mesial temporal lobe epilepsy.

Cumulative evidence suggests that programmed cell death (apoptosis) may contribute to the progressive hippocampal sclerosis seen in patients with refractory mesial temporal lobe epilepsy (MTLE). The endoplasmic reticulum (ER) stress-mediated cell apoptotic pathway has recently emerged as a vital intrinsic pathway, but the molecular mechanisms underlying this process in the epileptic brain remain unclear. We investigated inositol-requiring protein 1α (IRE1α)-mediated ER stress pro-and anti-apoptotic signaling pathways in resected hippocampi from 32 patients with intractable MTLE.

Preliminary explorations of the role of mitochondrial proteins in refractory epilepsy: some findings from comparative proteomics.

Approximately 20-30% of patients with epilepsy continue to have seizures despite carefully monitored treatment with antiepileptic drugs. The mechanisms that underlie why some patients are responsive and others prove resistant to antiepileptic drugs are poorly understood. Increasing evidence supports a role for altered mitochondrial function in the pathogenesis of epilepsy.