Associated Papers
Correcting tau isoform ratios with a long-acting antisense oligonucleotide alleviates 4R-tauopathy phenotypes.
Iwata-Endo K et al.
Molecular Therapy. Nucleic Acids, 2025
Regulation of DNA damage response by RNA/DNA-binding proteins: Implications for neurological disorders and aging.
Kodavati M et al.
Ageing Research Reviews, 2024
TDP-43 Proteinopathy and Tauopathy: Do They Have Pathomechanistic Links?
Riku Y et al.
International Journal of Molecular Sciences, 2022
ALS Genetics: Gains, Losses, and Implications for Future Therapies.
Kim G et al.
Neuron, 2020
Aberrant interaction between FUS and SFPQ in neurons in a wide range of FTLD spectrum diseases.
Ishigaki S et al.
Brain : a Journal of Neurology, 2020
Importance of Functional Loss of FUS in FTLD/ALS.
Ishigaki S et al.
Frontiers in Molecular Biosciences, 2018
Pathogenesis of Frontotemporal Lobar Degeneration: Insights From Loss of Function Theory and Early Involvement of the Caudate Nucleus.
Sobue G et al.
Frontiers in Neuroscience, 2018
Altered Tau Isoform Ratio Caused by Loss of FUS and SFPQ Function Leads to FTLD-like Phenotypes.
Ishigaki S et al.
Cell Reports, 2017
Familial behavioral variant frontotemporal dementia associated with astrocyte-predominant tauopathy.
Ferrer I et al.
Journal of Neuropathology and Experimental Neurology, 2015
Delineating the genetic heterogeneity of ALS using targeted high-throughput sequencing.
Kenna KP et al.
Journal of Medical Genetics, 2013
23881933 (PubMed )
Supplement: jmedgenet-2013-101795-s1.pdf
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