A Comprehensive Resource for Induced Pluripotent Stem Cells from Patients with Primary Tauopathies: Stem Cell Reports

SNARE Proteins Are Required for Macroautophagy: Cell

https://t.co/IyvZ3UmXdC

PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia:

New webinar coming next MONDAY‼️ Sarah Marzi from UK Dementia Research Institute @sj_marzi @UKDRI will be our next speaker on November 3rd. Check all the information in the flyer and add it to your calendar!

DDX3X acts as a selective dual switch regulator of mRNA translation in acute ER stress

We're excited to share our new pre-print, where @GizemTerzioglu_ et al. identify SHIP1, the protein encoded by the Alzheimer's disease risk gene INPP5D, as a regulator of endo-lysosome function and selective phagocytosis in human iPSC-derived microglia. https://t.co/iS2ixs9NTA

#EndAlz @alzassociation

1/ 🚨 New preprint from the lab! We show that #Frontotemporal #dementia-causing #tau mutations (#P301S, #S305N, IVS10+16) hyperactivate rDNA transcription, triggering nucleolar hyperactivity, stress, and neurotoxicity in diverse models. 🔗 https://t.co/pI8gokuvzG

A nice article in @washumedicine about our recent paper: https://t.co/WJWrHe729v

Our glial circadian atlas in AD and aging mice is now out in @NatureNeuro! Congrats to @patwsheehan for incredible work and to our collaborators @johnthefryer, @CarpeRibosomam, @darshan1s, Ron Anafi, and the team. @johnthefryer and I started this in 2019! https://t.co/AYnP0sCbGj

We can fix it! Adding more FAM151B-DT to cells reduces tau and alpha-synuclein aggregation. Making this a promising target for drug design for FTD and Parkinson’s disease @AFTDHope @MichaelJFoxOrg

When FAM151B-DT is silenced, tau and alpha-synuclein levels go up, and we detect more aggregation of these proteins. We think this is because FAM makes it harder for the cell to get the bad proteins into the trash

Of course FAM151B-DT was poorly characterized, so Arun got to work finding it is cytosolic and interacts with tau, alpha-synuclein, and a ton of proteins involved in protein clearance!

When looking for lncRNAs that change in FTD, one stood out that was reduced in human neuronal models and in FTD brains: FAM151B-DT 🧠🧫

New work from the lab shows that a novel non-coding RNA, FAM151B-DT, is a driver of tau and alpha-synuclein aggregation ⁦@washumedicine⁩ ⁦@RCFNeuro⁩ ⁦@WashUMedADRC⁩

After 18 years of transformative leadership, AFTD CEO Susan L-J Dickinson will retire in May 2026. From a team of 3 and a $400K budget to 50+ staff, 600+ volunteers, and $12M dedicated to FTD progress — Susan’s vision has shaped AFTD’s growth and impact. The Board of Directors

Surprisingly, the RNA and protein changes we see in the FTD microglia are similar to those in the brains and CSF from people with FTD caused by tau mutations. So we can use this model to help find ways to switch disease signatures to healthy signatures 🧠🧫

A mutation that causes FTD, IVS+10, destabilizes cytoskeletonal networks in microglia and reduces uptake of tau aggregates

Tau isn’t just a neuronal protein. We find it in microglia too! (but at much lower levels)

Excited to share new work from the lab showing that FTD causing mutations in tau cause widespread defects in microglia function ⁦@WashUMedADRC⁩ ⁦@RCFNeuro⁩ ⁦@AFTDHope⁩