Publications by authors named "Julia Dyckow"

Article Synopsis
  • Heterozygous mutations in the TBK1 gene are linked to neurodegenerative diseases like ALS and FTD, with most patients carrying harmful loss-of-expression mutations.
  • The study focused on the p.E696K missense variant of TBK1, which doesn't completely stop protein expression but disrupts its interaction with the autophagy protein optineurin.
  • Research showed that this mutation leads to early dysfunction in neuron recycling processes, resulting in damaged lysosomes and eventually causing a progressive motor neuron disease, highlighting potential therapeutic targets for treatment.
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Queuosine (Q) is a modified nucleoside at the wobble position of specific tRNAs. In mammals, queuosinylation is facilitated by queuine uptake from the gut microbiota and is introduced into tRNA by the QTRT1-QTRT2 enzyme complex. By establishing a Qtrt1 knockout mouse model, we discovered that the loss of Q-tRNA leads to learning and memory deficits.

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Multiple sclerosis (MS) is a progressive inflammatory demyelinating disease of the CNS. Increasing evidence suggests that vulnerable neurons in MS exhibit fatal metabolic exhaustion over time, a phenomenon hypothesized to be caused by chronic hyperexcitability. Axonal Kv7 (outward-rectifying) and oligodendroglial Kir4.

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Neural-derived signals are crucial regulators of CNS vascularization. However, whether the vasculature responds to these signals by means of elongating and branching or in addition by building a feedback response to modulate neurodevelopmental processes remains unknown. In this study, we identified bidirectional crosstalk between the neural and the vascular compartment of the developing CNS required for oligodendrocyte precursor cell specification.

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Multiple sclerosis is an autoimmune disease of the CNS in which both genetic and environmental factors are involved. Genome-wide association studies revealed more than 200 risk loci, most of which harbour genes primarily expressed in immune cells. However, whether genetic differences are translated into cell-specific gene expression profiles and to what extent these are altered in patients with multiple sclerosis are still open questions in the field.

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