The Haass lab Twitter account | š©šŖ @DZNE_de @SyNergy_Cluster | š¬AD, FTLD & microglia research | šµļø PI Christian Haass (signed -CH) | š¬ Tweets by @LisdeW_
DZNE, Munich, Germany
Joined March 2021
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Haass lab retweeted
š¢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.
š ema.europa.eu/en/news/leqembā¦
Haass lab retweeted
šØNEW PAPER ALERT šØ Our paper just got published in @ImmunityCP ! From Munich with š„Ø Check it out here: cell.com/immunity/fulltext/Sā¦ @Seiji_Kaji, @StefanBerghoff, Mikael Simons #apoe #Alzheimers #microglia 1/9
Haass lab retweeted
šØ 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
Haass lab retweeted
Wir sprechen in der neuesten Resonator-Podcastfolge Ć¼ber 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/reā¦
#Alzheimer #DZNE #Lecanemab #Podcast
Haass lab retweeted
Nick Fox making the case that excess brain volume loss associated with Lecanemab (or other effective mABās) is associated with the removal of āspace-occupyingā structures, as amyloid plaques occupy ~6-8% of the cortex in autopsy studies. #AAIC24
Haass lab retweeted
Out today, the statement by @DZNE_en experts on the @EMA_News decision on #lecanemab dzne.de/en/im-fokus/meldungeā¦ .
Haass lab retweeted
Homozygosity for R47H in TREM2 and the Risk of Alzheimerās 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:
1ā£ Does not contribute to AĪ² overproduction but instead disrupts AĪ² clearance
2ā£ Leads to the accumulation of amyloid plaques
3ā£ Is associated with a high risk of symptomatic Alzheimerās 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 AĪ²-removing antibodies are shown to have efficacy at the preclinical stage."
Link to paper > nejm.org/doi/pdf/10.1056/NEJā¦
Haass lab retweeted
APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimerās Disease nejm.org/doi/full/10.1056/NEā¦
Haass lab retweeted
'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
Haass lab retweeted
Big announcement today!š¢ 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.šyoutube.com/watch?v=tHhVov_Iā¦ā¦ā¦ #HFA #videoportrait #alzheimersdisease #alzheimersresearch #cellbiology
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/scitā¦ (1/8)
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 ā all phenotypes can be rescued by treatment with PTV:PGRN (7/8)
