Michael Ward

Michael Ward

@michael-e-ward.bsky.social

Physician scientist studying the biology of neurodegenerative disorders. ORCID ID: 0000-0002-5296-8051

1.4K followers589 following74 posts

Amazing paper by Carlton and Issacs - Seems that ANXA11 has a number of tricks up its sleeve!

Jez Carlton@jezcarlton.bsky.social

Great collaboration with @adrianisaacs.bsky.social showing coordinated role for FTD/ALS proteins CHMP2B and ANXA11 in membrane repair! Well done Catherine Heffner, Georgina Starling, Lorian Cobra Straker and Pippa Hawes! @crick.ac.uk, @ukdri.ac.uk, @kingslsm.bsky.social. www.cell.com/developmenta...

Michael Ward reposted

Michael Ward reposted

📣 new preprint multimodal atlas. Imaging + scRNA, 57M cells. 🧬🔬 Cells are complex dynamical systems — but most ways we measure them destroy them. We asked: how does live imaging compare to scRNA-seq, the field’s gold std? The answer surprised us 🧵 www.biorxiv.org/content/10.6...

Michael Ward reposted

Giving a talk? Don't waste time with "practice talks". Stay in slide sorter view & practice 3 things for each slide: 1. What point/s do I want to convey with this slide (</=3). 2. What's the 1-line summary of this slide? 3. What is the transition to the next slide? Something doesn't fit? FIX IT

Michael Ward reposted

Triple the science budget AND fix agency governance. TLDR: Those are the two essential things we must fix in US science. Get the president out of the science agencies, no presidential influence beyond appointment, stop the attacks on the civil service, restore Congressional power and oversight.

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Having done my neurology residency at UCSF and postdoc at Gladstone, returning to the Bay is a bit of a homecoming for me. I'm looking forward to joining a community that includes many of my scientific heroes.

We're actively recruiting postdoctoral fellows with expertise in cell biology, microscopy, and computational biology. If that describes you or someone you know, please reach out directly or send me a CV

Nearly eleven years ago, I launched my own research lab at the NIH intramural research program. I'm grateful to the colleagues, mentors, and (above all) the trainees who made that period the most scientifically rewarding of my career.

We built a research program that I’m deeply proud of, and alongside collaborators both inside and outside of the NIH we made important discoveries about the basic biology of neurodegenerative diseases. The NIH is a genuinely special place.

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This work was led by three outstanding trainees: John Replogle, Jordan Marks, and Martin Fernandez. Their creativity and hard work made this possible, along with efforts from many others across multiple labs.

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TMEM106B is also a lysosomal protein. Its cleaved intra-luminal fibril core domain forms within the lysosome and serves as the direct precursor to these fibrils, which accumulate inside the very compartment responsible for their clearance.

In post-mortem FTLD-GRN brain, we find these intra-lysosomal fibrils associated with ruptured lysosomes. Reducing their formation or clearing them may represent a new therapeutic target for dementia.

Disease-associated variants in these genes drive neurotoxic TMEM106B amyloid fibril accumulation. A coding TMEM106B variant impairs fibril degradation, while GRN variants amplify accumulation through reduced intra-lysosomal progranulin, a lysosomal protein.

Michael Ward reposted

Check out the newest work from our, from Fabricio Nicola @fabricionicola.bsky.social on mouse jumping and spinal cell types. Excellent collab with @vulcnethologist.bsky.social www.biorxiv.org/content/10.6...

biorxiv.orgA spinal substrate for modular control of natural behaviorNatural behavior unfolds as coordinated sequences of body movements. This organization suggests that behavior may be built from discrete motor patterns, yet how such arrangements are implemented by neural circuits remains unknown. Here, we combined kinematic analysis, muscle recordings, genetically identified cell types, and closed-loop optogenetic perturbations to examine the organizational logic of natural gap-crossing jumps in mice. Jumping was characterized by a series of precisely defined phases and their associated modular motor patterns. The core phases, propulsion and flight, exhibited distinct signatures of neural control, including unique bursts of coordinated hindlimb muscle activity, differential tuning strategies for jump distance, and active requirements for spinal neural drive. Mapping activity across lumbar interneuron populations and functionally screening candidate cell types for their ability to drive coordinated movement revealed that a population of dorsal excitatory dILB6 neurons can autonomously evoke coordinated multi-joint hindlimb flexion characteristic of the jumping flight phase, across behavioral contexts. These findings provide a specific cellular substrate for the long-standing concept of spinal modular motor control: a flexible, preconfigured motor template that the mammalian CNS can recruit and modulate to meet the demands of natural behavior. ### Competing Interest Statement The authors have declared no competing interest. Intramural Research Program of the National Institutes of Health (NIH)
Fabricio Nicola@fabricionicola.bsky.social

Mammals have hundreds of joints and muscles. Controlling them individually would be nearly impossible. How does the nervous system organize such complexity into coherent actions? Our new study explores this question through a natural behavior: jumping.

Michael Ward reposted

The most impt change at #NIH and to US science this year is bigger than grant cancellations— it’s how the agency is governed. For 75 years NIH has been largely independent of presidential control. That’s changed this year. New piece from me and @nataliebaviles.bsky.social in @nature.com 🧪

nature.comHow Congress can restore the independence of US scienceMembers must go beyond reinstating US government research spending and re-establish decentralized governance at the National Institutes of Health and other agencies.

Michael Ward reposted

A new #ScienceSignaling study offers insights into the KOLF2.IJ cell line, which is derived from induced pluripotent stem cells and has been proposed as a neuronal model for Alzheimer’s disease and related #dementia research. https://scim.ag/4aFNY9O

scim.agTemporal proteomic and phosphoproteomic dynamics during neuronal differentiation in the reference iPSC line KOLF2.1JTrace protein and phosphoprotein dynamics during neuronal differentiation in the iPSC-derived cell line model are described.

Michael Ward reposted

Michael Ward reposted

Michael Ward reposted

Michael Ward reposted

Michael Ward reposted

Begging PhD programs to agree on a common app with only letters of rec that writers upload once. These inane likert scales when students are applying to 15-20 programs is destroying my soul