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pro vyhledávání: '"Daniel J Fillingham"'
Autor:
Rachel Waller, Lynne Baxter, Daniel J Fillingham, Santiago Coelho, Jose M Pozo, Meghdoot Mozumder, Alejandro F Frangi, Paul G Ince, Julie E Simpson, J Robin Highley
Publikováno v:
PLoS ONE, Vol 14, Iss 1, p e0210888 (2019)
Deep subcortical lesions (DSCL) of the brain, are present in ~60% of the ageing population, and are linked to cognitive decline and depression. DSCL are associated with demyelination, blood brain barrier (BBB) dysfunction, and microgliosis. Microglia
Externí odkaz:
https://doaj.org/article/bf9ba81364ba489bb1902dc093d4234a
An interaction between synapsin and C9orf72 regulates excitatory synapses and is impaired in ALS/FTD
Autor:
Claudia S. Bauer, Rebecca N. Cohen, Francesca Sironi, Matthew R. Livesey, Thomas H. Gillingwater, J. Robin Highley, Daniel J. Fillingham, Ian Coldicott, Emma F. Smith, Yolanda B. Gibson, Christopher P. Webster, Andrew J. Grierson, Caterina Bendotti, Kurt J. De Vos
Publikováno v:
Bauer, C S, Cohen, R N, Sironi, F, Livesey, M R, Gillingwater, T H, Highley, J R, Fillingham, D J, Coldicott, I, Smith, E F, Gibson, Y B, Webster, C P, Grierson, A J, Bendotti, C & De Vos, K J 2022, ' An interaction between synapsin and C9orf72 regulates excitatory synapses and is impaired in ALS/FTD ', Acta Neuropathologica, vol. 144, pp. 437–464 .
Dysfunction and degeneration of synapses is a common feature of amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD). A GGGGCC hexanucleotide repeat expansion in the C9ORF72 gene is the main genetic cause of ALS/FTD (C9ALS/FTD). The re
Autor:
Daniel J. Fillingham, Paul G. Ince, Santiago Coelho, Meghdoot Mozumder, Jose M. Pozo, Lynne Baxter, Rachel Waller, Alejandro F. Frangi, J. Robin Highley, Julie E. Simpson
Publikováno v:
PLoS ONE
Publons
PLoS ONE, Vol 14, Iss 1, p e0210888 (2019)
Publons
PLoS ONE, Vol 14, Iss 1, p e0210888 (2019)
Deep subcortical lesions (DSCL) of the brain, are present in ~60% of the ageing population, and are linked to cognitive decline and depression. DSCL are associated with demyelination, blood brain barrier (BBB) dysfunction, and microgliosis. Microglia