Caffeine and adenosine A(2A) receptor inactivation decrease striatal neuropathology in a lentiviral-based model of Machado-Joseph disease. - Test2 - elhamkhani - TriplyDB

Caffeine and adenosine A(2A) receptor inactivation decrease striatal neuropathology in a lentiviral-based model of Machado-Joseph disease.

Caffeine and adenosine A(2A) receptor inactivation decrease striatal neuropathology in a lentiviral-based model of Machado-Joseph disease.

http://www.wikidata.org/entity/Q42437833

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Structure-Bioactivity Relationships of Methylxanthines: Trying to Make Sense of All the Promises and the Drawbacks Early synaptic deficits in the APP/PS1 mouse model of Alzheimer's disease involve neuronal adenosine A2A receptors.RNA interference mitigates motor and neuropathological deficits in a cerebellar mouse model of Machado-Joseph disease ATP as a multi-target danger signal in the brain.Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma.Caloric restriction blocks neuropathology and motor deficits in Machado-Joseph disease mouse models through SIRT1 pathway.Ataxin-3 protein and RNA toxicity in spinocerebellar ataxia type 3: current insights and emerging therapeutic strategies.Unravelling Endogenous MicroRNA System Dysfunction as a New Pathophysiological Mechanism in Machado-Joseph Disease.Health benefits of methylxanthines in neurodegenerative diseases.How does adenosine control neuronal dysfunction and neurodegeneration?The neuroprotective effects of caffeine in neurodegenerative diseases.Adenosine A2A Receptors Modulate α-Synuclein Aggregation and Toxicity.Neuropeptide Y mitigates neuropathology and motor deficits in mouse models of Machado-Joseph disease.Re-establishing ataxin-2 downregulates translation of mutant ataxin-3 and alleviates Machado-Joseph disease.Novel candidate blood-based transcriptional biomarkers of Machado-Joseph disease.Caffeine alleviates progressive motor deficits in a transgenic mouse model of spinocerebellar ataxia.The role of microglia in the progression of glaucomatous neurodegeneration- a review.Calpain inhibition reduces ataxin-3 cleavage alleviating neuropathology and motor impairments in mouse models of Machado-Joseph disease.Caffeine and Modafinil Ameliorate the Neuroinflammation and Anxious Behavior in Rats during Sleep Deprivation by Inhibiting the Microglia Activation.Beneficial Role of Coffee and Caffeine in Neurodegenerative Diseases: A Minireview.Purinergic Receptors in Neurological Diseases With Motor Symptoms: Targets for Therapy.

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Caffeine and adenosine A(2A) receptor inactivation decrease striatal neuropathology in a lentiviral-based model of Machado-Joseph disease.

http://www.wikidata.org/entity/Q42437833

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2013 nî lūn-bûn

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2013年论文

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Caffeine and adenosine A(2A) r ...... del of Machado-Joseph disease.

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Caffeine and adenosine A(2A) r ...... del of Machado-Joseph disease.

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Caffeine and adenosine A(2A) r ...... del of Machado-Joseph disease.

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Annals of Neurology

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Caffeine and adenosine A(2A) r ...... del of Machado-Joseph disease.

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Ana T Simões

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Luís Pereira de Almeida

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Nélio Gonçalves

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P2860

The ubiquitin-specific protease Usp4 regulates the cell surface level of the A2A receptor

Glial cells as intrinsic components of non-cell-autonomous neurodegenerative disease

Adenosine A2A receptors and basal ganglia physiology

Ataxin-3 interactions with rad23 and valosin-containing protein and its associations with ubiquitin chains and the proteasome are consistent with a role in ubiquitin-mediated proteolysis

CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1

Early changes in Huntington's disease patient brains involve alterations in cytoskeletal and synaptic elements

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

Blockade of A2A adenosine receptors prevents basic fibroblast growth factor-induced reactive astrogliosis in rat striatal primary astrocytes

Nuclear localization of ataxin-3 is required for the manifestation of symptoms in SCA3: in vivo evidence

Spinocerebellar ataxia type 3 phenotypically resembling parkinson disease in a black family.

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655-666

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10.1002/ANA.23866

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5

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73

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Rodrigo A. Cunha

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2013-04-26T00:00:00Z

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236460701

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corpus striatum