The Haass lab Twitter account | šŸ‡©šŸ‡Ŗ @DZNE_de @SyNergy_Cluster | šŸ”¬AD, FTLD & microglia research | šŸ•µļø PI Christian Haass (signed -CH) | šŸ’¬ Tweets by @LisdeW_

Joined March 2021
45 Photos and videos
13 Jan 2025
Last post on X: we officially moved to bsky. Come find us there!
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šŸ“¢The CHMP recommends authorising a new treatment for early #AlzheimersDisease in the EU. Leqembi is intended for treatment of mild dementia and cognitive impairment in a restricted patient population with a specific genetic make-up. šŸ‘‰ ema.europa.eu/en/news/leqemb…
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🚨 Just out in Theranostics: ā˜¢ļø we developed a new microglia specific Cu64-labeled TREM2-PET radiotracer ā˜¢ļø importantly this antibody based tracer has an integrated brain shuttle system (hTfR) to cross the blood-brain barrier. thno.org/v14p6319.htm #Theranostics

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Wir sprechen in der neuesten Resonator-Podcastfolge über den aktuellen Stand der Alzheimerforschung. Zu Gast ist Christian Haas vom @DZNE_de und es geht auch um neue Medikamente. Ganze Sendung: resonator-podcast.de/2024/re… #Alzheimer #DZNE #Lecanemab #Podcast
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Nick Fox making the case that excess brain volume loss associated with Lecanemab (or other effective mAB’s) is associated with the removal of ā€œspace-occupyingā€ structures, as amyloid plaques occupy ~6-8% of the cortex in autopsy studies. #AAIC24
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Homozygosity for R47H in TREM2 and the Risk of Alzheimer’s Disease Another AD-relevant publication @NEJM this week. TREM2 variants like R47H may induce partial loss of function by interfering with binding of ligands such as low-density lipoprotein (LDL), apolipoprotein E (ApoE), and clusterin (CLU). R47H homozygosity: 1⃣ Does not contribute to Aβ overproduction but instead disrupts Aβ clearance 2⃣ Leads to the accumulation of amyloid plaques 3⃣ Is associated with a high risk of symptomatic Alzheimer’s disease (OR=97.1; 95% CI=23.5-401.1). Conclusion: "The high risk in R47H homozygotes underscores the necessity for early intervention if treatments such as Aβ-removing antibodies are shown to have efficacy at the preclinical stage." Link to paper > nejm.org/doi/pdf/10.1056/NEJ…
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'Mis-localization of endogenous #TDP43 leads to #ALS-like early-stage metabolic dysfunction and progressive motor deficits' Yiying Hu, Alexander Hruscha, Chenchen Pan...Bettina Schmid @DZNE_en @SyNergy_Cluster bit.ly/45vRfEk
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Big announcement today!šŸ“¢ We are very pleased to present the new video portrait with Hector Fellow Prof. Dr. Dr. h.c. Christian Haass and his research on Alzheimer's disease.šŸ‘‰youtube.com/watch?v=tHhVov_I……… #HFA #videoportrait #alzheimersdisease #alzheimersresearch #cellbiology
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Interested in translational science? 🧪 Our team at #DZNE Munich is seeking a technician for the GA-VAX project. Your work could directly contribute to clinical trials with #C9orf72 #ALS patients. Apply now and join our team! #Jobs #Research jobs.dzne.de/de/jobs/101347/…

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6 Jun 2024
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/scit… (1/8)
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6 Jun 2024
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)
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6 Jun 2024
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)
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