Haass Lab

Microglia replacement halts the progression of microgliopathy in mice and humans Colony-stimulating factor 1 receptor (CSF1R) is primarily expressed in microglia. Its monoallelic mutation causes CSF1R-associated microgliopathy (CAMP), a major form of adult-onset leukoencephalopath...

Microglia replacement halts the progression of microgliopathy in mice and humans @science.org www.science.org/doi/10.1126/...

GitHub - lmu-osc/safeguar.de-hackathon Contribute to lmu-osc/safeguar.de-hackathon development by creating an account on GitHub.

​Hackathon: Data Under Threat/Data Rescuing in #München

The LMU OSC runs a hackathon to support the #SciOp #SafeguardingResearch initiative: Rescuing research data that is deleted by the Trump administration.
📅 07/08/25 from 16 – 19 (only in-person)
👉 Details and signup: github.com/lmu-osc/safe...

Photo of ceremony.

Photo of ceremony.

Congratulations to Christian Haass (@haasslab.bsky.social)! He receives an honorary doctorate from the University of Eastern Finland for 30+ years of groundbreaking Alzheimer’s research on beta-amyloid proteins and new therapeutic approaches. 📸: UFE/Raija Törrönen & UFE/Niko Jouhkimainen

A word cloud made from flagged terms in terminated NIH grant proposals. The most prominent words in large font include “trans,” “diverse,” “diversity,” “minority,” “sex,” “expression,” “mental health,” “gender,” and “women.” Other visible terms include “LGBTQ,” “racial,” “underrepresented,” “disability,” “barriers,” “black,” “equity,” “health equity,” “vaccine,” “bias,” and “intersectionality.” The word cloud highlights terms related to identity, inclusion, and marginalized communities.

HAPPY PRIDE 🏳️‍🌈

Under Trump, research using terms like “Trans,” “LGBTQ,” & “Gender identity” is being defunded. These terms reflect real people who deserve science that includes them.

Stand with us to protect LGBTQ+ science from political erasure.
grant-watch.us/nih-data.html
@rcmedphys.bsky.social

How does APOE change your risk of developing Alzheimer's disease? At least partially by changing the function of immune cells in your brain 🧠🧬

New paper out in @natcomms.nature.com today: www.nature.com/articles/s41...

@ukdri.ac.uk @kingsioppn.bsky.social @imperialbrains.bsky.social

Map of Germany with the Clusters of Excellence

The #ClustersOfExcellence have been selected: today, the Excellence Commission approved 70 projects for funding. 45 clusters will continue and 25 will be newly established. Funding starts on 1 Jan 2026 for 7 years, with €539 million per year. The full list: www.dfg.de/resource/blo... 1/3

🎉 Major achievement for #LMU in the Excellence Strategy: All seven proposed Clusters of Excellence have successfully passed the review process and will be funded for seven years as of 2026. An outstanding result! 🎉 #ExcellenceCluster #LMUMunich #research Read more here: www.lmu.de/en/newsroom/...

💭 Our PhD & Postdoc reps initiated visits to our Technology Hubs for our researchers and kicked off with a visit to our Single-Cell and Spatial Transcriptome Hubs last week.

👋 Thanks Arek Kendirli, Janos Groh, Clara de la Rosa del Val, and Simon Frerich for hosting the first event of the series!

We've been studying mechanisms of resilience that protect lysosomes from damage and wrote a review on the topic. We consider lysosomal stress and damage on a spectrum. Please help me share as this is my first post 😀 and I don't have many followers! 🙏 Open Access: www.embopress.org/doi/full/10....

Excited to share our latest work with Denali Therapeutics as Deep Piction. Using our proprietary clearing & imaging, we’ve mapped the full targeting profile of brain-penetrating transport vehicles (ATVs) in both whole mouse bodies and monkey brains. nature.com/articles/s41...

Physiological shedding and C-terminal proteolytic processing of TMEM106B Genetic variants in TMEM106B, coding for a transmembrane protein of unknown function, have been identified as critical genetic modulators in various n…

Our new paper on the proteolytic processing of TMEM106B is out in @cp-cellreports.bsky.social! TMEM106B undergoesphysiological shedding and additional C-terminal trimming. The new luminal-domain antibody is commercially available!
www.sciencedirect.com/science/arti...

We did it and now it is published: A highly Lewy-fold selective and quantitative Synuclein Aggregate Amplification Assay (SAA). Huge thanks to the amazing teams at MODAG GmbH, LMU Munich, and Bologna University!
rdcu.be/eaISM

👋 Meet our PhD and Postdoc Representatives

💭 The voice of our PhD students and Postdocs. A point of contact for feedback, questions, criticism, and improvements. And they organize extracurricular activities! Meet @angelikadannert.bsky.social, Clara, Lis and Nathalie.

🔗 Read more: lnkd.in/dKtzshqr

Microglia degrade Alzheimer’s amyloid-beta deposits extracellularly via digestive exophagy Jacquet et al. shows that microglia use digestive exophagy to engage large Aβ deposits that cannot be phagocytosed, forming acidic extracellular compartments on the aggregates into which lysosomal enz...

This is really interesting. Known for a long time lysosomal enzymes are secreted- it’s the principle of cross correction for lysosomal
Storage diseases. However the idea lysosomes are released or degrading plaques extracellularly is 🤯. Do they differ from EVs/EPs?

www.cell.com/cell-reports...

Big congrats to the winners, including Marvin Reich, PhD student co-supervised by our lab in a nice collab with @haasslab.bsky.social

NLRP3-mediated glutaminolysis controls microglial phagocytosis to promote Alzheimer’s disease progression How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...

I am thrilled to share our latest article that has been published in @cp-immunity.bsky.social. We describe a new role for NLRP3 outside of its #inflammasome complex, where it can regulate microglial #metabolism & key metabolites that affect the epigenetic landscape(1)
www.cell.com/immunity/ful...

Multimodal synapse analysis reveals restricted integration of transplanted neurons remodeled by TREM2 https://www.biorxiv.org/content/10.1101/2025.01.31.635250v1

Alpha-Synuclein co-pathology in Alzheimer's Disease drives tau accumulation https://www.biorxiv.org/content/10.1101/2025.01.24.634706v1

Very happy to announce that the PaquetLab is now on Bluesky. We are excited to connect with everyone interested in our research and present updates on our work and lab activities! Our lab engineers 3-dimensional models of #human-brain-tissue and the #BBB and applies them to investigate ...

In summary, we show that a novel therapeutic approach of single-dose peripheral AAV-induced delivery of a brain penetrant biotherapeutic molecule, can replace PGRN protein levels in the brain and ameliorate disease-relevant phenotypes! (8/8)

What about a human model system? To assess this we also created a novel human TMEM106B/GRN DKO iPSC model that recapitulates TDP-43 pathology, neurodegeneration and lysosomal abnormalities – all phenotypes can be rescued by treatment with PTV:PGRN (7/8)

Increased PGRN levels lead to a reduction of TDP-43 pathology, decreased neurodegeneration and an amelioration of motor deficits and behavioural phenotypes! (6/8)

Applying AAV(L):bPGRN to Tmem106b x Grn double KO mice, we show that a single injection can restore progranulin levels in neurons, microglia, astrocytes and endothelial cells for a prolonged time (5/8)

In this study, we use a novel therapeutic approach, combining protein replacement with gene therapy. We exploit a liver-transducible AAV (AAV(L)), which induces brain penetrant (b)PGRN expression in hepatocytes and releases it to the blood to be transcytosed into the brain (4/8)

To get around this our collaborators at Denali Therapeutics have recently designed a novel protein replacement approach in the form of a brain penetrant version of PGRN that shuttles through the BBB via transferrin receptor-mediated transcytosis (3/8)

FTLD-GRN patients have a life-long gene-dose dependent reduction in PGRN levels and could benefit from protein replacement. However, recent approaches that directly target the brain with AAVs, require invasive procedures and show potentially serious adverse side effects... (2/8)

Peripheral expression of brain-penetrant progranulin rescues pathologies in mouse models of frontotemporal lobar degeneration Peripheral AAV-mediated delivery of brain-penetrant PGRN rescues TDP-43 pathology, neurodegeneration, and motor phenotypes in FTLD-GRN models.

(REPOST) Can we achieve protein replacement in the brain using a single dose gene therapy approach, without infecting the brain? Yes we can! Read it here in our latest paper by @marvin_reich in collaboration with Denali Therapeutics science.org/doi/10.1126/... (1/8)