Brain network analysis reveals hemispheric aberrant topology in patients with idiopathic REM sleep behavior disorder.

Idiopathic REM sleep behavior disorder (iRBD) is recognized as a prodromal stage of neuro-degenerative disease. While brain network analysis is a well-documented approach for characterizing disease-related dysfunctions, the specific patterns in iRBD, particularly those related to hemispheric aberrations remain largely unexplored. To address this gap, this study investigated the topological abnormalities of multi-band EEG networks in patients with iRBD.

Task Cortical Connectivity Reveals Different Network Reorganizations between Mild Stroke Patients with Cortical and Subcortical Lesions.

Accumulating efforts have been made to investigate cognitive impairment in stroke patients, but little has been focused on mild stroke. Research on the impact of mild stroke and different lesion locations on cognitive impairment is still limited. To investigate the underlying mechanisms of cognitive dysfunction in mild stroke at different lesion locations, electroencephalograms (EEGs) were recorded in three groups (40 patients with cortical stroke (CS), 40 patients with subcortical stroke (SS), and 40 healthy controls (HC)) during a visual oddball task.

Novel nano-carriers with N-formylmethionyl-leucyl-phenylalanine-modified liposomes improve effects of C16-angiopoietin 1 in acute animal model of multiple sclerosis.

Gradual loss of neuronal structure and function due to impaired blood-brain barrier (BBB) and neuroinflammation are important factors in multiple sclerosis (MS) progression. Our previous studies demonstrated that the C16 peptide and angiopoietin 1 (Ang-1) compound (C + A) could modulate inflammation and vascular protection in many models of MS. In this study, nanotechnology and a novel nanovector of the leukocyte chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLP) were used to examine the effects of C + A on MS.

Brain network analysis reveals convergent and divergent aberrations between mild stroke patients with cortical and subcortical infarcts during cognitive task performing.

Although consistent evidence has revealed that cognitive impairment is a common sequela in patients with mild stroke, few studies have focused on it, nor the impact of lesion location on cognitive function. Evidence on the neural mechanisms underlying the effects of mild stroke and lesion location on cognitive function is limited. This prompted us to conduct a comprehensive and quantitative study of functional brain network properties in mild stroke patients with different lesion locations.

Neurocircuitry underlying the antidepressant effect of retrograde facial botulinum toxin in mice.

Backgrounds: Botulinum toxin type A (BoNT/A) is extensively applied in spasticity and dystonia as it cleaves synaptosome-associated protein 25 (SNAP25) in the presynaptic terminals, thereby inhibiting neurotransmission. An increasing number of randomized clinical trials have suggested that glabellar BoNT/A injection improves depressive symptoms in patients with major depressive disorder (MDD). However, the underlying neuronal circuitry of BoNT/A-regulated depression remains largely uncharacterized.

Co-Application of C16 and Ang-1 Improves the Effects of Levodopa in Parkinson Disease Treatment.

Background: Levodopa is regarded as a standard medication in Parkinson disease (PD) treatment. However, long-term administration of levodopa leads to levodopa-induced dyskinesia (LID), which can markedly affect patient quality of life. Previous studies have shown that neuroinflammation in the brain plays a role in LID and increases potential neuroinflammatory mediators associated with the side effects of levodopa.

C16 Peptide and Ang-1 Improve Functional Disability and Pathological Changes in an Alzheimer's Disease Model Associated with Vascular Dysfunction.

Alzheimer's disease (AD) is a neurological disorder characterized by neuronal cell death, tau pathology, and excessive inflammatory responses. Several vascular risk factors contribute to damage of the blood-brain barrier (BBB), secondary leak-out of blood vessels, and infiltration of inflammatory cells, which aggravate the functional disability and pathological changes in AD. Growth factor angiopoietin-1 (Ang-1) can stabilize the endothelium and reduce endothelial permeability by binding to receptor tyrosine kinase 2 (Tie2).

Pathological Gait Signatures of Post-stroke Dementia With Toe-Off and Heel-to-Ground Angles Discriminate From Alzheimer's Disease.

Given the limited power of neuropsychological tests, there is a need for a simple, reliable means, such as gait, to identify mild dementia and its subtypes. However, gait characteristics of patients with post-stroke dementia (PSD) and Alzheimer's disease (AD) are unclear. We sought to describe their gait signatures and to explore gait parameters distinguishing PSD from post-stroke non-dementia (PSND) and patients with AD.

Structural and Functional Deficits in Patients with Poststroke Dementia: A Multimodal MRI Study.

Although many neuroimaging studies have reported structural and functional abnormalities in the brains of patients with cognitive impairments following stroke, little is known about the pattern of such brain reorganization in poststroke dementia (PSD). The present study was aimed at investigating alterations in spontaneous brain activity and gray matter volume (GMV) in PSD patients. We collected T1-weighted and resting-state functional magnetic resonance imaging data from 20 PSD patients, 24 poststroke nondementia (PSND) patients, and 21 well-matched normal controls (NCs).

Adjusting vascular permeability, leukocyte infiltration, and microglial cell activation to rescue dopaminergic neurons in rodent models of Parkinson's disease.

Animal studies have indicated that increased blood-brain barrier (BBB) permeability and inflammatory cell infiltration are involved during the progression of Parkinson's disease (PD). This study used C16, a peptide that competitively binds to integrin αβ and inhibits inflammatory cell infiltration, as well as angiopoietin-1 (Ang-1), an endothelial growth factor crucial for blood vessel protection, to reduce inflammation and improve the central nervous system (CNS) microenvironment in murine models of PD. The combination of C16 and Ang-1 yielded better results compared to the individual drugs alone in terms of reducing dopaminergic neuronal apoptosis, ameliorating cognitive impairment, and electrophysiological dysfunction, attenuating inflammation in the CNS microenvironment, and improving the functional disability in PD mice or rats.

Inhibition of endoplasmic reticulum stress reverses synaptic plasticity deficits in striatum of DYT1 dystonia mice.

Background And Objective: Striatal plasticity alterations caused by endoplasmic reticulum (ER) stress is supposed to be critically involved in the mechanism of DYT1 dystonia. In the current study, we expanded this research field by investigating the critical role of ER stress underlying synaptic plasticity impairment imposed by mutant heterozygous Tor1a in a DYT1 dystonia mouse model.

Methods: Heterozygous Tor1a mouse model for DYT1 dystonia was established.

Combined treatment with C16 peptide and angiopoietin-1 confers neuroprotection and reduces inflammation in 3-nitropropionic acid-induced dystonia mice.

Dystonia is a disorder associated with abnormalities in many brain regions including the basal ganglia and cerebellum. The toxin 3-Nitropropionic acid (3-NP) can induce neuropathologies in the mice striatum and nigra substance, including excitotoxicity, neuroinflammation, and extensive neuronal atrophy, characterized by progressive motor dysfunction, dystonia, and memory loss, mimicking those observed in humans. We established a mouse model of dystonia by administering 3-NP.

Altered Functional Connectivity of Hippocampal Subfields in Poststroke Dementia.

Background: The hippocampus (HP) plays a critical role in memory and orientational functions and is functionally heterogeneous along the longitudinal anterior-posterior axis. Although the previous study has reported volumetric atrophy in hippocampal subfields of patients with poststroke dementia (PSD), how the functional connectivity (FC) is altered in these subfields remains unclear.

Purpose: To examine the FC changes of the HP subfields in patients with PSD.

Atrophic Pattern of Hippocampal Subfields in Post-Stroke Demented Patient.

Background: Previous studies have demonstrated that hippocampal atrophy is a hallmark of dementia and can be used to predict the outcome of post-stroke demented (PSD) patients. The hippocampus consists of several subfields but their involvement in the pathophysiology of the PSD remains unclear.

Objective: The present study aimed to investigate volumetric alterations of hippocampal subfields in patients with PSD.

A Signature of Five Long Non-Coding RNAs for Predicting the Prognosis of Alzheimer's Disease Based on Competing Endogenous RNA Networks.

Long non-coding RNAs (lncRNAs) play important roles in the pathogenesis of Alzheimer's disease (AD). However, the functions and regulatory mechanisms of lncRNA are largely unclear. Herein, we obtained 3,158 lncRNAs by microarray re-annotation.

An APP mutation family exhibiting white matter hyperintensities and cortical calcification in East China.

Heterozygous amyloid precursor protein (APP) mutations cause hereditary cerebral amyloid angiopathy (CAA) and autosomal dominant Alzheimer's disease (AD). This study aimed at reporting an APP mutation and its associated clinical and neuroimaging features. The proband and her family members presented with memory loss, psychiatric, and visual symptoms.

Gait characteristics and clinical relevance of hereditary spinocerebellar ataxia on deep learning.

Background: Deep learning has always been at the forefront of scientific research. It has also been applied to medical research. Hereditary spinocerebellar ataxia (SCA) is characterized by gait abnormalities and is usually evaluated semi-quantitatively by scales.

Pitfalls in the diagnosis and initial management of acute cerebral venous thrombosis.

Cerebral venous thrombosis is an important etiology of stroke in young patients. Its clinical manifestations are variable and based on different involved venous or sinus processes. Cerebral venous thrombosis could mimic ischemic infarction and is easy to misdiagnose.

Angiopoietin-1 and ανβ3 integrin peptide promote the therapeutic effects of L-serine in an amyotrophic lateral sclerosis/Parkinsonism dementia complex model.

Amyotrophic lateral sclerosis (ALS) is an adult disorder of neurodegeneration that manifests as the destruction of upper and lower motor neurons. Beta-N-methylamino-L-alanine (L-BMAA), an amino acid not present in proteins, was found to cause intraneuronal protein misfolding and to induce ALS/Parkinsonism dementia complex (PDC), which presents symptoms analogous to those of Alzheimer's-like dementia and Parkinsonism. L-serine suppresses the erroneous incorporation of L-BMAA into proteins in the human nervous system.

Guillain-Barré Syndrome and Low Back Pain: Two Cases and Literature Review.

To describe the clinical, electrophysiological, and lumbar magnetic resonance imaging (MRI) features of two cases of atypical Guillain-Barré syndrome (GBS). Methods We reported two GBS variant cases with initial and prominent symptoms of low back pain. We analysed their clinical, electrophysiological, and lumbar MRI features.

HIV/AIDS-related knowledge awareness and risk behaviors among injection drug users in Maanshan, China: a cross-sectional study.

Background: Unsafe injection practices significantly increase the risk of human immunodeficiency virus (HIV) infection among injection drug users (IDUs). Little is known about how demographic characteristics of IDUs are linked to HIV-related risk behaviors in the central regions of China.

Methods: A cross-sectional survey was conducted at Mandatory Detoxification Centers (MDCs) and the community in Maanshan, China.

Acrylamide inhibits nerve sprouting induced by botulinum toxin type A.

Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective and safe therapy for strabismus and focal dystonia. However, muscular weakness is temporary and after 3-4 months, muscle strength usually recovers because functional recovery is mediated by nerve sprouting and reconstruction of the neuromuscular junction.