Haass lab

The Haass lab Twitter account | 🇩🇪 @DZNE_de @SyNergy_Cluster | 🔬AD, FTLD & microglia research | 🕵️ PI Christian Haass (signed -CH) | 💬 Tweets by @LisdeW_

[Haass lab @Haass_Lab]

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

[EU Medicines Agency @EMA_News]

📢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.

👉 https://t.co/0rUpn7K7ri

[Lena Spieth @LenaSpieth]

🚨NEW PAPER ALERT 🚨 Our paper just got published in @ImmunityCP ! From Munich with 🥨 Check it out here: https://t.co/CSmlm3EJ0r @Seiji_Kaji, @StefanBerghoff, Mikael Simons #apoe #Alzheimers #microglia 1/9

[MatthiasBrendel @matbrendel]

🚨 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. https://t.co/14bpnFmuRM #Theranostics

[Helmholtz @helmholtz_de]

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: https://t.co/JkZ3v3Nca1

#Alzheimer #DZNE #Lecanemab #Podcast

[RikOssenkoppele @RikOssenkoppele]

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

[Gabor Petzold @Gaborpetzold]

Out today, the statement by @DZNE_en experts on the @EMA_News decision on #lecanemab https://t.co/YSf1c7agHr .

[RikOssenkoppele @RikOssenkoppele]

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 > https://t.co/xIJg6Rnqq8

[Celeste Karch @karchlab]

APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimer’s Disease https://t.co/kBCduToUAs

[Molecular Neurodegeneration @MolNeuro]

'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

https://t.co/j7XCVJF0Ve

[Hector Fellow Academy @HFA_academy]

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.👉https://t.co/6aYa03dXx0…… #HFA #videoportrait #alzheimersdisease #alzheimersresearch #cellbiology

[Dieter Edbauer @dieter_edbauer]

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
https://t.co/qDSNZefM5D

[Haass lab @Haass_Lab]

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)

[Haass lab @Haass_Lab]

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 https://t.co/Url2eTyRk1 (1/8)

[Haass lab @Haass_Lab]

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)