Haass lab

Last post on X: we officially moved to bsky. Come find us there!

📢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. 👉 ema.europa.eu/en/news/leqemb…

🚨NEW PAPER ALERT 🚨 Our paper just got published in @ImmunityCP ! From Munich with 🥨 Check it out here: cell.com/immunity/fullt… @Seiji_Kaji, @StefanBerghoff, Mikael Simons #apoe #Alzheimers #microglia 1/9

🚨 Just out in Theranostics: ☢️ we developed a new microglia specific Cu64-labeled TREM2-PET radiotracer ☢️ importantly this antibody based tracer has an integrated brain shuttle system (hTfR) to cross the blood-brain barrier. thno.org/v14p6319.htm #Theranostics

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/res207-zu… #Alzheimer #DZNE #Lecanemab #Podcast

Nick Fox making the case that excess brain volume loss associated with Lecanemab (or other effective mAB’s) is associated with the removal of “space-occupying” structures, as amyloid plaques occupy ~6-8% of the cortex in autopsy studies. #AAIC24

Out today, the statement by @DZNE_en experts on the @EMA_News decision on #lecanemab dzne.de/en/im-fokus/me… .

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/10.105…

APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimer’s Disease nejm.org/doi/full/10.10…

'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

Big announcement today!📢 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.👉youtube.com/watch?v=tHhVov……… #HFA #videoportrait #alzheimersdisease #alzheimersresearch #cellbiology

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…

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)

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/sc… (1/8)