A dramatic increase of C1q protein in the CNS during normal aging. - Wikidata - wikimedia - TriplyDB

A dramatic increase of C1q protein in the CNS during normal aging.

A dramatic increase of C1q protein in the CNS during normal aging.

http://www.wikidata.org/entity/Q37093902

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Rediscovering area CA2: unique properties and functions Emerging and Novel Functions of Complement Protein C1q Astrocytes Control Synapse Formation, Function, and Elimination Microglia communication: Parallels between aging and Alzheimer's disease Central Nervous System: (Immunological) Ivory Tower or Not?Microglia contribute to circuit defects in Mecp2 null mice independent of microglia-specific loss of Mecp2 expression Microglia: Dynamic Mediators of Synapse Development and Plasticity.Cortical plasticity induced by transplantation of embryonic somatostatin or parvalbumin interneurons.Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation.A lack of immune system genes causes loss in high frequency hearing but does not disrupt cochlear synapse maturation in mice.Neurotoxic reactive astrocytes are induced by activated microglia.C1 Complex: An Adaptable Proteolytic Module for Complement and Non-Complement Functions A complement-microglial axis drives synapse loss during virus-induced memory impairment.New insights on the role of microglia in synaptic pruning in health and disease Sexually divergent induction of microglial-associated neuroinflammation with hippocampal aging.The intersection of amyloid beta and tau at synapses in Alzheimer's disease Maternal complement C1q and increased odds for psychosis in adult offspring.Versatility of the complement system in neuroinflammation, neurodegeneration and brain homeostasis Are there roles for brain cell senescence in aging and neurodegenerative disorders?Prenatal stress is a vulnerability factor for altered morphology and biological activity of microglia cells APOE Stabilization by Exercise Prevents Aging Neurovascular Dysfunction and Complement Induction.Understanding How Exercise Promotes Cognitive Integrity in the Aging Brain.Cecal Ligation and Puncture Results in Long-Term Central Nervous System Myeloid Inflammation.Complement receptor 2 is up regulated in the spinal cord following nerve root injury and modulates the spinal cord response.Fine-mapping of the human leukocyte antigen locus as a risk factor for Alzheimer disease: A case-control study.Peripheral challenge with a viral mimic upregulates expression of the complement genes in the hippocampus.Do glia drive synaptic and cognitive impairment in disease?C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation.Cerebral Response to Peripheral Challenge with a Viral Mimetic.C1q propagates microglial activation and neurodegeneration in the visual axis following retinal ischemia/reperfusion injury.Fundamental role of C1q in autoimmunity and inflammation Peripherally restricted viral challenge elevates extracellular glutamate and enhances synaptic transmission in the hippocampus Aging Shapes the Population-Mean and -Dispersion of Gene Expression in Human Brains Novel allele-dependent role for APOE in controlling the rate of synapse pruning by astrocytes.C1q induction and global complement pathway activation do not contribute to ALS toxicity in mutant SOD1 mice.Complement component 3 (C3) expression in the hippocampus after excitotoxic injury: role of C/EBPβ.Age-related changes in cerebellar and hypothalamic function accompany non-microglial immune gene expression, altered synapse organization, and excitatory amino acid neurotransmission deficits.Complement and microglia mediate early synapse loss in Alzheimer mouse models.Maternal immune activation and abnormal brain development across CNS disorders.Glia: guardians, gluttons, or guides for the maintenance of neuronal connectivity?

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A dramatic increase of C1q protein in the CNS during normal aging.

http://www.wikidata.org/entity/Q37093902

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on August 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

A dramatic increase of C1q protein in the CNS during normal aging.

@en

A dramatic increase of C1q protein in the CNS during normal aging.

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type

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A dramatic increase of C1q protein in the CNS during normal aging.

@en

A dramatic increase of C1q protein in the CNS during normal aging.

@nl

prefLabel

A dramatic increase of C1q protein in the CNS during normal aging.

@en

A dramatic increase of C1q protein in the CNS during normal aging.

@nl

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JNEUROSCI.1333-13.2013

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Journal of Neuroscience

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A dramatic increase of C1q protein in the CNS during normal aging

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Alexander H Stephan

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Andrea J Tenner

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Ben A Barres

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Daniel V Madison

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Deborah A Fraser

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Dominic S Berns

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Emilie A Lovelett

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Hui-Hsin Tsai

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Laurence Coutellier

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Leo Kim

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P2860

Complement C1q activates canonical Wnt signaling and promotes aging-related phenotypes

The cell-adhesion G protein-coupled receptor BAI3 is a high-affinity receptor for C1q-like proteins

Rab3B protein is required for long-term depression of hippocampal inhibitory synapses and for normal reversal learning

The classical complement cascade mediates CNS synapse elimination

Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner

The complement system: an unexpected role in synaptic pruning during development and disease

Trans-synaptic interaction of GluRdelta2 and Neurexin through Cbln1 mediates synapse formation in the cerebellum

Neurotrypsin cleaves agrin locally at the synapse

Complement: a key system for immune surveillance and homeostasis

Developments of a water-maze procedure for studying spatial learning in the rat

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13460-13474

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scholarly article

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10.1523/JNEUROSCI.1333-13.2013

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33

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33

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Jose Maria Mateos

David H Rowitch

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2013-08-01T00:00:00Z

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23946404

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3742932

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