Adrian Isaacs Lab
@adrianisaacslab
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https://t.co/x1yYnHFij1 London laboratory investigating disease mechanisms of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia
London, England
Joined January 2017
Go Yash!! @yashgx
A day in the life of our superstar tech Yash! recorded for @DHSCgovuk
https://t.co/rjwtfRkPjL
@UKDRI @UCLBrainScience @in2scienceUK
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Our open access opinion in @Brain1878 on the disappointing C9 ASO trials and next steps to deliver an effective treatment for C9ALS/FTD co-written with @AlexCammack @RubikaBalendra @UKDRI @UCLIoN
https://t.co/A4kgL7j5bA
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Delighted to see our study led by @milioto_carmelo revealing a neuroprotective ECM signature in C9FTD/ALS published! Thanks to @mndassoc @UKDRI and many others!
nature.com
Nature Neuroscience - C9orf72 ALS/FTD polyGR and polyPR knock-in mice show cortical hyperexcitability and motor neuron loss accompanied by an increase in extracellular matrix proteins in the spinal...
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After failure of ASO trials targeting C9orf72 sense repeats also targeting antisense repeats is now vital. Our new preprint shows a potential approach using CRISPR-CasRx @UKDRI @UCLIoN @AlexCammack
biorxiv.org
The most common genetic cause of both frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is a G4C2 repeat expansion in intron 1 of the C9orf72 gene. This repeat expansion undergoes...
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Really excited about our latest preprint, where we uncovered a neuroprotective role for neuronal polyunsaturated fatty acids in FTD and ALS. Led by @AshlingGiblin and @AlexCammack
https://t.co/NIm2FmGZV5 1/9
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Genome-wide RNA binding analysis of C9orf72 poly(PR) dipeptides, excited for this preprint with @ule_lab & @adrianisaacslab to be out!
biorxiv.org
An intronic GGGGCC repeat expansion in C9orf72 is a common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. The repeats are transcribed in both sense and antisense direct...
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Our new preprint identifies genome wide the RNAs bound by C9orf72 polyPR a great collaboration with @ule_lab and @ShorterLab led by @RubikaBalendra @UKDRI
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NEWS: Researchers led by Prof Adrian Isaacs (@isaacs_adrian, UK DRI at UCL) have developed a biomarker to track the success of therapies targeting the most common genetic cause of frontotemporal dementia & amyotrophic lateral sclerosis 🧬 Read more 👉 https://t.co/tAQCiL2DMG
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New preprint on developing a sensitive Simoa-based CSF biomarker for C9orf72FTD/ALS great collaboration with @FTDtalk @GENFI1 @jonrohrer @WaveLifeSci @ajh1269 led by @katiewilson1604 and Eszter Katona
medrxiv.org
A GGGGCC repeat expansion in the C9orf72 gene is the most common cause of genetic frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). As potential therapies targeting the repeat...
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Our latest paper shows a novel role for insulin signalling in C9orf72FTD/ALS https://t.co/7IXII08gXM great work from @AtilanoMagda @UKDRI @UCLIoN
elifesciences.org
Modulation of insulin signalling could be an effective therapeutic approach against hexanucleotide repeat expansion related to c9ALS/FTD neurodegenerative diseases.
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C9orf72 polyGR is another FTD/ALS-linked protein whose phase separation is altered by arginine methylation - and levels in brain correlate with disease duration - just out in print and great work from @lougittings and @BoeynaemsSteven
https://t.co/qttirXqteQ
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Nice preview by @katiewilson1604
Why does the RNA helicase DDX3X have opposing effects on RAN translation of different repeat sequences? Find out in our @NeuroCellPress preview: Relax, don't RAN translate it https://t.co/obUrYoWLuZ
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Congratulations to Dr @JackHumphrey_ and Dr @lougittings who graduated today! Past students of the Isaacs lab 🎓🍾
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Now on bioRxiv: "FUS ALS-causative mutations impact FUS autoregulation and the processing of RNA-binding proteins through intron retention” https://t.co/vZHLbVi36w Thanks to everyone in @FrattaPietro, @adrianisaacslab, @VincentPlagnol , Marc-David Ruepp and Irene Bozzoni labs.
biorxiv.org
Mutations in the RNA binding protein FUS cause amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disease in which the loss of motor neurons induces progressive weakness and death...
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Super happy to see my first, first author paper in print! 🎉👩🏻🔬🙌🏼Thanks to @lashleylab , @adrianisaacslab and @tammarynlashley
link.springer.com
Acta Neuropathologica Communications - Frontotemporal lobar degeneration (FTLD) is pathologically subdivided based on the presence of particular pathological proteins that are identified in...
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The Isaacs lab celebrating the diversity in the lab with our first International Lunch at the @UKDRI Featuring Spanish croquettes, Italian carbonara, Indian chutney, Swedish potato salad, Hungarian stew, English sausage rolls & German kaiserschmarrn!😋 🤤
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Our new paper by @MoensT shows C9orf72 repeat-mediated translational repression and toxicity are rescued by EIF1A https://t.co/FJVkfrdcGq
@UKDRI
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Congratulations to the two new doctors in the lab - @JackHumphrey_ and @lougittings. Both have passed their PhD vivas this month! 🎉🍾📚🧠
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Our new paper: mutant CHMP2B alters neuronal endolysosome trafficking which is rescued by TMEM106B ASOs! https://t.co/lN4meFbUtR
@Brain1878 @UKDRI
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Come find out about our research into frontotemporal dementia at this free event at #UCL today! Free to attend & lots of interactive activities. Everyone welcome!
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