scholarly journals CDC50A dependent phosphatidylserine exposure induces inhibitory post-synapse elimination by microglia

2020 ◽  
Author(s):  
Jungjoo Park ◽  
Eunji Jung ◽  
Seung-Hee Lee ◽  
Won-Suk Chung
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Knockout Mice ◽  
Neurological Disorders ◽  
Conditional Knockout ◽  
Synapse Elimination ◽  
Specific Loss ◽  
Microglial Phagocytosis ◽  
Phosphatidylserine Exposure ◽  
The Central Nervous System

AbstractGlia contribute to synapse elimination through phagocytosis in the central nervous system. Despite important roles during development and neurological disorders, the “eat-me” signal that initiates glia-mediated phagocytosis of synapses remains largely elusive. Here, by generating inducible conditional knockout mice of Cdc50a, we induced stable exposure of phosphatidylserine in the neuronal outer membrane. Surprisingly, acute Cdc50a deletion in neurons causes specific loss of inhibitory post-synapses without affecting other synapses, thereby generating excessive excitability with appearance of seizure. Ablating microglia or deleting microglial Mertk rescues the loss of inhibitory post-synapses, indicating that microglial phagocytosis is responsible for inhibitory post-synapse elimination. Moreover, inhibitory post-synapses in normal juvenile brains also use phosphatidylserine for synapse pruning by microglia, suggesting that phosphatidylserine may serve as a general “eat-me” signal for inhibitory post-synapse elimination.One Sentence SummaryCdc50a dependent phosphatidylserine exposure functions as an “eat-me” signal for microglia-dependent inhibitory post-synapse elimination

scholarly journals Meningitis Caused by Salmonella Newport in a Five-Year-Old Child

2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Ana De Malet ◽  
Sheila Ingerto ◽  
Israel Gañán
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Disorders ◽  
Invasive Disease ◽  
Salmonella Typhi ◽  
Gram Negative ◽  
Negative Bacillus ◽  
Salmonella Newport ◽  
Gram Negative Bacillus ◽  
The Central Nervous System

Salmonella Newport is a Gram-negative bacillus belonging to the Enterobacteria family and the nontyphi Salmonella (NTS), usually related to gastroenteritis. Main difference between NTS and Salmonella typhi is that the last one evolves to an invasive disease easier than NTS. These can progress to bacteremias in around 5% of cases and secondary focuses can appear occasionally, as in meningitis. An infection of the central nervous system is uncommon, considering its incidence in 0.6–8% of the cases; most of them are described in developing countries and mainly in childhood, especially neonates. Bacterial meningitis by NTS mostly affects immunosuppressed people in Europe. Prognosis is adverse, with a 50% mortality rate, mainly due to complications of infection: hydrocephalus, ventriculitis, abscesses, subdural empyema, or stroke. Choice antibiotic treatments are cefotaxime, ceftriaxone, or ceftazidime. The aim of this paper is to present a case of meningitis caused by Salmonella Newport diagnosed in a five-year-old girl living in a rural area of the province of Ourense (Spain), with favorable evolution and without neurological disorders.

scholarly journals Insights Into the Role of CSF1R in the Central Nervous System and Neurological Disorders

2021 ◽  
Vol 13 ◽  
Author(s):  
Banglian Hu ◽  
Shengshun Duan ◽  
Ziwei Wang ◽  
Xin Li ◽  
Yuhang Zhou ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Colony Stimulating Factor ◽  
Loss Of Function ◽  
Axonal Spheroids ◽  
The Central Nervous System ◽  
Stimulating Factor

The colony-stimulating factor 1 receptor (CSF1R) is a key tyrosine kinase transmembrane receptor modulating microglial homeostasis, neurogenesis, and neuronal survival in the central nervous system (CNS). CSF1R, which can be proteolytically cleaved into a soluble ectodomain and an intracellular protein fragment, supports the survival of myeloid cells upon activation by two ligands, colony stimulating factor 1 and interleukin 34. CSF1R loss-of-function mutations are the major cause of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and its dysfunction has also been implicated in other neurodegenerative disorders including Alzheimer’s disease (AD). Here, we review the physiological functions of CSF1R in the CNS and its pathological effects in neurological disorders including ALSP, AD, frontotemporal dementia and multiple sclerosis. Understanding the pathophysiology of CSF1R is critical for developing targeted therapies for related neurological diseases.

scholarly journals Features of nervous system damage in antiphospholipid syndrome

2021 ◽  
Vol 15 (4) ◽  
pp. 404-414
Author(s):  
O. N. Voskresenskaya ◽  
V. O. Bitsadze ◽  
J. Kh. Khizroeva ◽  
T. A. Sukontseva ◽  
M. V. Tretyakova ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Antiphospholipid Syndrome ◽  
Neurological Disorders ◽  
Molecular Mimicry ◽  
Transverse Myelitis ◽  
Autoimmune Process ◽  
The Central Nervous System ◽  
Interdisciplinary Interaction

Antiphospholipid syndrome (APS) is an autoimmune process that increases the risk of arterial and venous thrombosis. The mechanism of damage to the central nervous system (CNS) can be not only due to thrombosis, but also antiphospholipid antibodies (APA) circulating in the peripheral blood. The latter can damage the cerebral vascular endothelium, alter the resistance of the blood-brain barrier and penetrate into the central nervous system, exerting a damaging effect on astroglia and neurons, as evidenced by the release of neurospecific proteins into the peripheral bloodstream. The role of APS in developing cerebral ischemia, migraine, epilepsy, chorea, transverse myelitis, multiple sclerosis, cognitive impairment and mental disorders, as well as the peripheral nervous system is described. It should also be noted about a role of APS for emerging neurological disorders in COVID-19, enabled apart from thrombogenesis due to APA via 2 potential mechanisms - molecular mimicry and neoepitope formation. Further study of the APS pathogenesis and interdisciplinary interaction are necessary to develop effective methods for patient management.

scholarly journals Sirtuin 2 (SIRT2): Confusing Roles in the Pathophysiology of Neurological Disorders

2021 ◽  
Vol 15 ◽  
Author(s):  
Xiuqi Chen ◽  
Wenmei Lu ◽  
Danhong Wu
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Rapid Growth ◽  
Nicotinamide Adenine Dinucleotide ◽  
Neurological Disorders ◽  
Potential Role ◽  
Therapeutic Strategies ◽  
Nicotinamide Adenine ◽  
The Central Nervous System ◽  
The Brain

As a type of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, sirtuin 2 (SIRT2) is predominantly found in the cytoplasm of cells in the central nervous system (CNS), suggesting its potential role in neurological disorders. Though SIRT2 is generally acknowledged to accelerate the development of neurological pathologies, it protects the brain from deterioration in certain circumstances. This review summarized the complex roles SIRT2 plays in the pathophysiology of diverse neurological disorders, compared and analyzed the discrete roles of SIRT2 in different conditions, and provided possible explanations for its paradoxical functions. In the future, the rapid growth in SIRT2 research may clarify its impacts on neurological disorders and develop therapeutic strategies targeting this protein.

scholarly journals Clinical and biochemical predictors of neurological disorders

2020 ◽  
Vol 4 (35) ◽  
pp. 34-39
Author(s):  
I. Yu. Serikova ◽  
G. I. Shumacher ◽  
E. N. Vorobyova ◽  
I. A. Batanina ◽  
R. I. Vorobyov
Keyword(s):  
Lipid Peroxidation ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurological Disorders ◽  
Protein S ◽  
Nerve Tissue ◽  
S 100 ◽  
The Central Nervous System ◽  
Peroxidation Processes ◽  
The City

The aim of this study is to identify clinical and biochemical predictors of neurological disorders in adolescents who have suffered mild perinatal damage of the central nervous system. We examined 120 adolescents (62 girls and 58 boys) aged 13–16 years, who were hospitalized in the city Children’s Neurological Department. It was found that adolescents with perinatal lesions of the central nervous system, activated lipid peroxidation processes and revealed an increase in the concentration of protein S 100, which in the future could lead to the development of neurodegeneration processes. In addition, a positive correlation between the lipid peroxidation processes nd the concentration of the nerve tissue damage marker was revealed. The results indicate that the level of neurospecific protein — protein S 100, parameters of the oxidant‑antioxidant system, perinatal factors can be used as predictors of chronic nervous tissue processes.

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