Research group at the MRC Mitochondrial Biology Unit, University of Cambridge. Interested in all things neurodegeneration, mitochondrial dysfunction, in vivo genetics, Drosophila, mitophagy, mtDNA, calcium, gut-brain axis etc
Alex Whitworth lab
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Which itself was informed by your earlier study with NCLX: www.nature.com/articles/s41...
We are pleased that our article on Ataxin-2 and the integrated stress response in C9orf72 ALS/FTD is finally published in full. A lot of hard work from members of the lab, including @comeflywithjo.bsky.social, and our collaborators
link.springer.com/article/10.1...
A new preprint from the lab led by a talented PhD student Niall Wilson and supported by amazing collaborators Sovan Sarkar, Tetsushi Kataura, Elton Zeqiraj, G. Vignir Helgason, Ian Ganley, and Agnieszka Bronowska
#AMPK is the key cellular sensor of #NAD 👇🏼👇🏼👇🏼
www.biorxiv.org/content/10.6...
Great review on an exciting field - emerging technologies to treat mitochondrial diseases, which have potential application to other conditions such as neurodegeneration.
Was intrigued when I saw this initiative launched a little while back. Delighted to see it is working well. Maybe it’ll be the beginning of redressing the balance of power with the publishing houses and help support ECRs and junior faculty.
Fantastic work Elrod Lab and collaborators!
👏🎉
Congrats @davetree.bsky.social
For short talks, I’d say practice talks are good because they force you to ‘find the words’ that will convey the message while keeping to time.
But these 3 points are where you should always start.
You just inadvertently forgot to mention our previous work on exactly this area a couple of years ago:
www.cell.com/cell-reports...
Same thing works in flies 🪰
You just inadvertently forgot to mention our previous work on exactly this area a couple of years ago:
www.cell.com/cell-reports...
Same thing works in flies 🪰
Alex Whitworth lab
Ryan West
Alex Whitworth lab
Alex Whitworth lab
Alex Whitworth lab
Alex Whitworth lab
Alex Whitworth lab
Alex Whitworth lab
Alex Whitworth lab
Korolchuk Lab
Dysregulation of intracellular calcium is reported in Alzheimer’s disease. Here the authors show that loss of the mitochondrial Na+ /Ca2+ exchanger, NCLX – primary route of mitochondrial calcium efflu...
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are fatal, early-onset neurodegenerative diseases. The most common genetic cause of FTD and ALS is a G4C2 hexanucleotide repeat ex...
link.springer.com
Twyning et al. show using a single in vivo platform that reducing mitochondrial calcium
uptake via MCU or increasing efflux via NCLX is beneficial across a variety of different
disease models. These f...
Twyning et al. show using a single in vivo platform that reducing mitochondrial calcium
uptake via MCU or increasing efflux via NCLX is beneficial across a variety of different
disease models. These f...
www.cell.com
Genetic ablation of neuronal mitochondrial calcium uptake impedes Alzheimer’s disease progression
John Elrod and colleagues
link.springer.com/article/10.1...
We are pleased to share a new review published in Cell Reports Medicine @cellpress.bsky.social: “Emerging therapeutic strategies for mitochondrial DNA-related diseases”
Full article: doi.org/10.1016/j.xc...
#Mitochondria #mtDNA #GeneTherapy #GenomeEditing #RareDiseases #TranslationalMedicine
Congratulations to David Tree, our 2025 Established Educator Teaching Excellence Award winner, on his promotion to Professor! To hear more about his journey from genetics to educational leadership, join him for his open inaugural lecture at Brunel University London:
Paying peer reviewers works.
Expanded Fast & Fair experiment @biologyopen.bsky.social:
• 5.5 vs 37.7 working days to decision with reviews
• ~3 vs ~9 reviewer invitations per manuscript
• no reduction in editor-assessed review quality
• similar acceptance rates
www.biorxiv.org/content/10.6...
Subhojit Roy MD, PhD
London Mitochondrial Centre
Biochemical Society
Loss of mCa2+ efflux capacity contributes to the pathogenesis and progression of Alzheimer’s disease (AD) by promoting mitochondrial Ca2+ (mCa2+) overload. Here, we utilized loss-of-function genetic m...
