61,959 results match your criteria neuronal dysfunction

Mild hypothermia facilitates mitochondrial transfer from astrocytes to injured neurons during oxygen-glucose deprivation/reoxygenation.

Neurosci Lett 2021 May 7:135940. Epub 2021 May 7.

Department of Anesthesiology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China. Electronic address:

Mitochondrial dysfunction is now considered an important sign of neuronal death during cerebral ischemia/reperfusion (I/R) injury. Studies have shown that the transfer of mitochondria from astrocytes to injured neurons contributes to endogenous neuroprotection after stroke. Basic and clinical studies have shown that mild hypothermia exerts a clear protective effect on neurons after cerebral ischemic injury, but the role of mild hypothermia in this endogenous neuroprotective mechanism remains unclear. Read More

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Chaperone-mediated autophagy controls the turnover of E3 ubiquitin ligase MARCHF5 and regulates mitochondrial dynamics.

Autophagy 2020 Dec 1:1-16. Epub 2020 Dec 1.

Department of Neurology, First Affiliated Hospital of GuangZhou Medical University, Guangzhou, Guangdong, China.

As a highly dynamic organelle, mitochondria undergo constant fission and fusion to change their morphology and function, coping with various stress conditions. Loss of the balance between fission and fusion leads to impaired mitochondria function, which plays a critical role in the pathogenesis of Parkinson disease (PD). Yet the mechanisms behind mitochondria dynamics regulation remain to be fully illustrated. Read More

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December 2020

Cerebrospinal fluid biomarker panel for synaptic dysfunction in Alzheimer's disease.

Alzheimers Dement (Amst) 2021 1;13(1):e12179. Epub 2021 May 1.

Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.

Introduction: Synaptic dysfunction and degeneration is one of the earliest events in Alzheimer's disease (AD) and the best correlate of cognitive decline. Thus, identification and validation of biomarkers reflecting synaptic degeneration to be used as prognostic biomarkers are greatly needed.

Method: Solid-phase extraction and parallel reaction monitoring mass spectrometry were used to quantify 17 synaptic proteins in CSF, in two cross-sectional studies including AD (n = 52) and controls (n = 37). Read More

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Effects of Amyloid Precursor Protein Overexpression on NF-κB, Rho-GTPase and Pro-Apoptosis Bcl-2 Pathways in Neuronal Cells.

Rep Biochem Mol Biol 2021 Jan;9(4):417-425

Division of Applied Biomedical Science and Biotechnology, School of Health Sciences, International Medical University, Kuala Lumpur, Malaysia.

Background: Alzheimer's disease (AD) is a neurodegenerative disorder that causes cognitive dysfunction. Previous studies have suggested that amyloid plaques, mainly comprising of amyloid-beta peptides, play a pivotal role in AD pathophysiology. This study focuses on the evaluation of the effects of amyloid precursor protein (APP) overexpression on NF-κB, Rho-GTPase and Bcl-2 mediated pro-apoptotic pathways in neuronal cells. Read More

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January 2021

The Renin-Angiotensin System Modulates Dopaminergic Neurotransmission: A New Player on the Scene.

Front Synaptic Neurosci 2021 22;13:638519. Epub 2021 Apr 22.

Centro de Altos Estudios en Ciencias Humanas y de la Salud, Universidad Abierta Interamericana, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.

Parkinson's disease (PD) is an extrapyramidal disorder characterized by neuronal degeneration in several regions of the peripheral and central nervous systems. It is the second most frequent neurodegenerative disease after Alzheimer's. It has become a major health problem, affecting 1% of the world population over 60 years old and 3% of people beyond 80 years. Read More

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Entorhinal Perfusion Predicts Future Memory Decline, Neurodegeneration, and White Matter Hyperintensity Progression in Older Adults.

J Alzheimers Dis 2021 May 3. Epub 2021 May 3.

Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA.

Background: Altered cerebral blood flow (CBF) has been linked to increased risk for Alzheimer's disease (AD). However, whether altered CBF contributes to AD risk by accelerating cognitive decline remains unclear. It also remains unclear whether reductions in CBF accelerate neurodegeneration and development of small vessel cerebrovascular disease. Read More

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An apparent core/shell architecture of polyQ aggregates in the aging C. elegans neuron.

Protein Sci 2021 May 9. Epub 2021 May 9.

Structural Biology Initiative, CUNY Advanced Science Research Center, New York, NY, United States.

Huntington's disease is caused by a polyglutamine (polyQ) expansion in the huntingtin protein which results in its abnormal aggregation in the nervous system. Huntingtin aggregates are linked to toxicity and neuronal dysfunction, but a comprehensive understanding of the aggregation mechanism in vivo remains elusive. Here, we examine the morphology of polyQ aggregates in C. Read More

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Pathophysiological relationship between COVID-19 and olfactory dysfunction: A systematic review.

Braz J Otorhinolaryngol 2021 Apr 25. Epub 2021 Apr 25.

Universidade Federal do Vale São Francisco (UNIVASF), Paulo Afonso, BA, Brazil.

Introduction: SARS-CoV-2 is the pathogen of COVID-19. The virus is composed of the spike, membrane and envelope. On physiological smell, odoriferous substances bind to proteins secreted by sustentacular cells in order to be processed by olfactory receptor neurons. Read More

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Microglial MT1 activation inhibits LPS-induced neuroinflammation via regulation of metabolic reprogramming.

Aging Cell 2021 May 8:e13375. Epub 2021 May 8.

Department of Neurology, Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Although its pathogenesis remains unclear, a number of studies indicate that microglia-mediated neuroinflammation makes a great contribution to the pathogenesis of PD. Melatonin receptor 1 (MT1) is widely expressed in glia cells and neurons in substantia nigra (SN). Read More

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Impaired neuronal activity and differential gene expression in STXBP1 encephalopathy patient iPSC-derived GABAergic neurons.

Hum Mol Genet 2021 May 7. Epub 2021 May 7.

Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan.

Syntaxin-binding protein 1 (STXBP1; also called MUNC18-1), encoded by STXBP1, is an essential component of the molecular machinery that controls synaptic vesicle docking and fusion. De novo pathogenic variants of STXBP1 cause a complex set of neurological disturbances, namely STXBP1 encephalopathy (STXBP1-E) that includes epilepsy, neurodevelopmental disorders, and neurodegeneration. Several animal studies have suggested the contribution of GABAergic dysfunction in STXBP1-E pathogenesis. Read More

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Extraction and Analysis of Dynamic Functional Connectome Patterns in Migraine Sufferers: A Resting-State fMRI Study.

Comput Math Methods Med 2021 17;2021:6614520. Epub 2021 Apr 17.

Artificial Intelligence and Neuro-Informatics Engineering (ARINE) Laboratory, School of Computer Engineering, Jiangsu Ocean University, Lianyungang 222002, China.

Migraine seriously affects the physical and mental health of patients because of its recurrence and the hypersensitivity to the environment that it causes. However, the pathogenesis and pathophysiology of migraine are not fully understood. We addressed this issue in the present study using an autodynamic functional connectome model (A-DFCM) with twice-clustering to compare dynamic functional connectome patterns (DFCPs) from resting-state functional magnetic resonance imaging data from migraine patients and normal control subjects. Read More

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DNA Hypermethylation Induced by L-Methionine Leads to Oligodendroglial and Myelin Deficits and Schizophrenia-Like Behaviors in Adolescent Mice.

Front Neurosci 2021 20;15:659853. Epub 2021 Apr 20.

Department of Histology and Embryology, Institute of Brain and Intelligence, Army Medical University (Third Military Medical University), Chongqing, China.

Increasing evidence has demonstrated that in addition to dysfunction of neuronal circuitry, oligodendroglial dysfunction and/or disruption of white matter integrity are found in the brains of patients with schizophrenia. DNA methylation, a well-established risk factor for schizophrenia, has been demonstrated to cause neuronal dysfunction; however, whether dysregulation of DNA methylation contributes to oligodendroglial/myelin deficits in the pathogenesis of schizophrenia remains unclear. In the present study, by using L-methionine-treated mice, we confirmed that mice with DNA hypermethylation exhibited an anxious phenotype, impaired sociability, and sensorimotor gating deficits. Read More

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An integrative network analysis framework for identifying molecular functions in complex disorders examining major depressive disorder as a test case.

Sci Rep 2021 May 6;11(1):9645. Epub 2021 May 6.

Advanced Glycoscience Research Cluster (AGRC), National University of Ireland Galway, Galway, Ireland.

In addition to the psychological depressive phenotype, major depressive disorder (MDD) patients are also associated with underlying immune dysregulation that correlates with metabolic syndrome prevalent in depressive patients. A robust integrative analysis of biological pathways underlying the dysregulated neural connectivity and systemic inflammatory response will provide implications in the development of effective strategies for the diagnosis, management and the alleviation of associated comorbidities. In the current study, focusing on MDD, we explored an integrative network analysis methodology to analyze transcriptomic data combined with the meta-analysis of biomarker data available throughout public databases and published scientific peer-reviewed articles. Read More

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Repetitive mild head trauma induces activity mediated lifelong brain deficits in a novel Drosophila model.

Sci Rep 2021 May 6;11(1):9738. Epub 2021 May 6.

Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, 30322, USA.

Mild head trauma, including concussion, can lead to chronic brain dysfunction and degeneration but the underlying mechanisms remain poorly understood. Here, we developed a novel head impact system to investigate the long-term effects of mild head trauma on brain structure and function, as well as the underlying mechanisms in Drosophila melanogaster. We find that Drosophila subjected to repetitive head impacts develop long-term deficits, including impaired startle-induced climbing, progressive brain degeneration, and shortened lifespan, all of which are substantially exacerbated in female flies. Read More

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Correlation Between Nitric Oxide and Urodynamics in Men With Bladder Outlet Obstruction.

Int Neurourol J 2021 May 6. Epub 2021 May 6.

Department of Urology, Bucheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Bucheon, Korea.

Purpose: To investigate the correlation between nitric oxide (NO) and urodynamics in men with bladder outlet obstruction (BOO) by analyzing nitric oxide synthase (NOS) in the urothelium.

Methods: We prospectively enrolled 25 men who planned to undergo surgical treatment for benign prostatic obstruction and identified as BOO in the preoperative urodynamics. Bladder tissue was taken during surgical prostate resection. Read More

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Neuro-Immune Cross-Talk in the Striatum: From Basal Ganglia Physiology to Circuit Dysfunction.

Front Immunol 2021 19;12:644294. Epub 2021 Apr 19.

Section of Neurology, Department of Medicine and Surgery, Università degli Studi di Perugia, Perugia, Italy.

The basal ganglia network is represented by an interconnected group of subcortical nuclei traditionally thought to play a crucial role in motor learning and movement execution. During the last decades, knowledge about basal ganglia physiology significantly evolved and this network is now considered as a key regulator of important cognitive and emotional processes. Accordingly, the disruption of basal ganglia network dynamics represents a crucial pathogenic factor in many neurological and psychiatric disorders. Read More

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Transcranial photobiomodulation prevents PTSD-like comorbidities in rats experiencing underwater trauma.

Transl Psychiatry 2021 May 5;11(1):270. Epub 2021 May 5.

Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.

Maladaptive fear memory processing after a traumatic event is a major contributor to the development of the comorbidities related to posttraumatic stress disorder (PTSD). An intervention to normalize this process could be a first-line treatment to prevent PTSD development. However, little progress has been made in identifying interventions that can prevent trauma survivors from developing PTSD. Read More

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CircPTK2-miR-181c-5p-HMGB1: a new regulatory pathway for microglia activation and hippocampal neuronal apoptosis induced by sepsis.

Mol Med 2021 05 5;27(1):45. Epub 2021 May 5.

Neuroscience Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, No. 88, Jiefang Road, Hangzhou, 310009, Zhejiang Province, China.

Background: Circular RNA hsa_circ_0008305 (circPTK2), miR-181c-5p and High mobility group box-1 (HMGB1) had a targeted regulatory relationship through bioinformatics analysis. This study explained the effects of these genes in microglia and sepsis mice.

Methods: Lipopolysaccharide (LPS) or Cecal Ligation and Puncture (CLP) was used to induce inflammation cell model or sepsis mouse model, as needed. Read More

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Gain of PITRM1 peptidase in cortical neurons affords protection of mitochondrial and synaptic function in an advanced age mouse model of Alzheimer's disease.

Aging Cell 2021 May 5:e13368. Epub 2021 May 5.

Department of Surgery, Columbia University, New York, NY, USA.

Mitochondrial dysfunction is one of the early pathological features of Alzheimer's disease (AD). Accumulation of cerebral and mitochondrial Aβ links to mitochondrial and synaptic toxicity. We have previously demonstrated the mechanism by which presequence peptidase (PITRM1)-mediated clearance of mitochondrial Aβ contributes to mitochondrial and cerebral amyloid pathology and mitochondrial and synaptic stress in adult transgenic AD mice overexpressing Aβ up to 12 months old. Read More

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Early functional changes associated with alpha-synuclein proteinopathy in engineered human neural networks.

Am J Physiol Cell Physiol 2021 May 5. Epub 2021 May 5.

Department of Neuromedicine and Movement Science, Faculty of Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norwaygrid.5947.f.

A patterned spread of proteinopathy represents a common characteristic of many neurodegenerative diseases. In Parkinson's disease (PD), misfolded forms of alpha-synuclein proteins accumulate in hallmark pathological inclusions termed Lewy bodies and Lewy neurites. Such protein aggregates seem to affect selectively vulnerable neuronal populations in the substantia nigra and to propagate within interconnected neuronal networks. Read More

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N-Acetylcysteine Ameliorates Neurotoxic Effects of Manganese Intoxication in Rats: A Biochemical and Behavioral Study.

Neurochem Res 2021 May 5. Epub 2021 May 5.

Department of Biophysics, Basic Medical Sciences Block II, Panjab University, Chandigarh, 160014, India.

Clinical and experimental evidences reveal that excess exposure to manganese is neurotoxic and leads to cellular damage. However, the mechanism underlying manganese neurotoxicity remains poorly understood but oxidative stress has been implicated to be one of the key pathophysiological features related to it. The present study investigates the effects associated with manganese induced toxicity in rats and further to combat these alterations with a well-known antioxidant N-acetylcysteine which is being used in mitigating the damage by its radical scavenging activity. Read More

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Examining the neural antecedents of tics in Tourette syndrome using electroencephalography.

J Neuropsychol 2021 May 5. Epub 2021 May 5.

School of Psychology, University of Nottingham, UK.

Tourette syndrome (TS) is a neurodevelopmental disorder characterized by the occurrence of motor and vocal tics. TS is associated with cortical-striatal-thalamic-cortical circuit dysfunction and hyper-excitability of cortical limbic and motor regions that lead to the occurrence of tics. Importantly, individuals with TS often report that their tics are preceded by premonitory sensory/urge phenomena (PU) that are described as uncomfortable bodily sensations that precede the execution of a tic and are experienced as an urge for motor discharge. Read More

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Investigation of Neuropathology after Nerve Release in Chronic Constriction Injury of Rat Sciatic Nerve.

Int J Mol Sci 2021 Apr 29;22(9). Epub 2021 Apr 29.

Division of Plastic and Reconstructive Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.

Peripheral compressive neuropathy causes significant neuropathic pain, muscle weakness and prolong neuroinflammation. Surgical decompression remains the gold standard of treatment but the outcome is suboptimal with a high recurrence rate. From mechanical compression to chemical propagation of the local inflammatory signals, little is known about the distinct neuropathologic patterns and the genetic signatures after nerve decompression. Read More

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The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction.

Biomedicines 2021 Apr 29;9(5). Epub 2021 Apr 29.

Department of Neurobiology and Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

Zinc is a highly abundant cation in the brain, essential for cellular functions, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. Read More

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Dysbiosis and Alzheimer's Disease: A Role for Chronic Stress?

Biomolecules 2021 Apr 30;11(5). Epub 2021 Apr 30.

Pharmacology Department, Faculty of Veterinary Medicine, Suez Canal University, Ismailia 41522, Egypt.

Alzheimer's disease (AD) is an incurable, neuropsychiatric, pathological condition that deteriorates the worth of geriatric lives. AD is characterized by aggregated senile amyloid plaques, neurofibrillary tangles, neuronal loss, gliosis, oxidative stress, neurotransmitter dysfunction, and bioenergetic deficits. The changes in GIT composition and harmony have been recognized as a decisive and interesting player in neuronal pathologies including AD. Read More

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Central Acting Hsp10 Regulates Mitochondrial Function, Fatty Acid Metabolism, and Insulin Sensitivity in the Hypothalamus.

Antioxidants (Basel) 2021 Apr 30;10(5). Epub 2021 Apr 30.

Junior Research Group Central Regulation of Metabolism, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany.

Mitochondria are critical for hypothalamic function and regulators of metabolism. Hypothalamic mitochondrial dysfunction with decreased mitochondrial chaperone expression is present in type 2 diabetes (T2D). Recently, we demonstrated that a dysregulated mitochondrial stress response (MSR) with reduced chaperone expression in the hypothalamus is an early event in obesity development due to insufficient insulin signaling. Read More

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The cAMP-phosphodiesterase 4 (PDE4) controls β-adrenoceptor- and CFTR-dependent saliva secretion in mice.

Biochem J 2021 May 4. Epub 2021 May 4.

University of South Alabama, Mobile, Alabama, United States.

Saliva, while often taken for granted, is indispensable for oral health and overall well-being, as inferred from the significant impairments suffered by patients with salivary gland dysfunction. Here, we show that treatment with several structurally-distinct PAN-PDE4 inhibitors, but not a PDE3 inhibitor, induces saliva secretion in mice, indicating it is a class-effect of PDE4 inhibitors. In anesthetized mice, while neuronal regulations are suppressed, PDE4 inhibition potentiates a β-adrenoceptor-induced salivation, that is ablated by the β-blocker Propranolol and is absent in homozygous ΔF508-CFTR mice lacking functional CFTR. Read More

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Galectin-1 ameliorates perioperative neurocognitive disorders in aged mice.

CNS Neurosci Ther 2021 May 4. Epub 2021 May 4.

Department of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.

Introduction: The incidence of perioperative neurocognitive disorders (PND) is higher in the elderly patients undergoing surgery. Microglia activation-mediated neuroinflammation is one of the hallmarks of PND. Galectin-1 has been identified as a pivotal modulator in the central nervous system (CNS), while the role of galectin-1 in PND induced by microglia-mediated neuroinflammation is still undetermined. Read More

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Broadening the phenotypic spectrum and physiological insights related to EIF2S3 variants.

Hum Mutat 2021 May 3. Epub 2021 May 3.

Centre de Génétique Humaine, Institut de Pathologie et de Génétique, 6041 Charleroi, Gosselies, Belgium.

Mental deficiency, epilepsy, hypogonadism, microcephaly and obesity (MEHMO) syndrome is a severe X-linked syndrome caused by pathogenic variants in EIF2S3. The gene encodes the γ subunit of the eukaryotic translation initiation factor-2, eIF2, essential for protein translation. A recurrent frameshift variant is described in severely affected patients while missense variants usually cause a moderate phenotype. Read More

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The intestinal luminal sources of α-synuclein: a gastroenterologist perspective.

Aaron Lerner

Nutr Rev 2021 May 3. Epub 2021 May 3.

A. Lerner is with the Zabludowicz Center for Autoimmune Diseases, Chaim Sheba Medical Center, Tel-Hashomer, Israel.

Parkinson's disease is characterized by nonmotor/motor dysfunction, midbrain dopaminergic neuronal death, and α-synuclein (aSN) deposits. The current hypothesis is that aSN accumulates in the enteric nervous system to reach the brain. However, invertebrate, vertebrate, and nutritional sources of aSN reach the luminal compartment. Read More

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