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「"Arzberger T "[Author]」の検索結果

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Cell-to-cell transmission of C9orf72 poly-(Gly-Ala) triggers key features of ALS/FTD.

Copathology in Progressive Supranuclear Palsy: Does It Matter?

Active poly-GA vaccination prevents microglia activation and motor deficits in a C9orf72 mouse model.

Alzheimer's disease pathology explains association between dementia with Lewy bodies and APOE-ε4/TOMM40 long poly-T repeat allele variants.

Loss of fragile X mental retardation protein precedes Lewy pathology in Parkinson's disease.

Poly-glycine-alanine exacerbates C9orf72 repeat expansion-mediated DNA damage via sequestration of phosphorylated ATM and loss of nuclear hnRNPA3.

Validation of the movement disorder society criteria for the diagnosis of 4-repeat tauopathies.

Early defects in translation elongation factor 1α levels at excitatory synapses in α-synucleinopathy.

Cortical circuit alterations precede motor impairments in Huntington's disease mice.

A protein quality control pathway regulated by linear ubiquitination.

How to apply the movement disorder society criteria for diagnosis of progressive supranuclear palsy.

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD.

Publisher Correction: ApoE attenuates unresolvable inflammation by complex formation with activated C1q.

ApoE attenuates unresolvable inflammation by complex formation with activated C1q.

Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE.

Proteomics and neuropathology identify ribosomes as poly-GR/PR interactors driving toxicity.

Analysis of RNA Expression Profiles Identifies Dysregulated Vesicle Trafficking Pathways in Creutzfeldt-Jakob Disease.

Effect of tau-pathology on charged multivesicular body protein 2b (CHMP2B).

Epigenome-wide DNA methylation profiling in Progressive Supranuclear Palsy reveals major changes at DLX1.

DNA methylation analysis on purified neurons and glia dissects age and Alzheimer's disease-specific changes in the human cortex.

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