Sadaf Amin

Transplantation of Human IPSC-derived Microglia Ameliorates Neuropathology and Circuit Dysfunction in Progranulin-Deficient Mice Frontotemporal dementia (FTD) is a major cause of early-onset neurodegeneration characterized by progressive behavioral, emotional, and cognitive decline. Progranulin haploinsufficiency, a leading gen...

Proud to announce our collaboration with @blurtonjoneslab.bsky.social & the Paz lab showing that transplanted human iPSC-derived microglia in a PGRN KO mouse model restores progranulin in microglia and rescues pathology, circuitry, and behavior. Preprint out now: www.biorxiv.org/cgi/content/...

Cell membrane stress upon viral infection induces expression and stabilization of host SMPDL3B, which, in turn, degrades cGAMP to suppress cGAS-STING signaling and promote viral replication @cp-immunity.bsky.social
www.cell.com/immunity/ful...

TDP-43 loss brings RNA to a twist ending - Nature Neuroscience In amyotrophic lateral sclerosis (ALS), nuclear depletion and cytoplasmic aggregation of the RNA-binding protein TDP-43 cause widespread dysregulation of mRNA splicing. Two recent studies have now rev...

New article @natneuro.nature.com by @yaleneuro.bsky.social Suzhou Yang & @kavliatyale.bsky.social Postdoc Fellow @zhenlei.bsky.social, highlighting studies by @frattalab.bsky.social Gitler & La Spada labs on the role of TDP-43 on mRNA 3' end in ALS @yalerna.bsky.social www.nature.com/articles/s41...

A single-cell, long-read, isoform-resolved case-control study of FTD reveals cell-type-specific and broad splicing dysregulation in human brain Belchikov et al. conducted a case-control study of splicing in frontotemporal dementia using long-read sequencing. They identified multiple splicing-dysregulation events, including cell-type-specific ...

Single cell isoform profiling by snISOrseq2 reveals broad splicing dysregulation across different cell types in Progranulin-deficient human FTD! Congrats to @hagentilgner.bsky.social & @liganlab.bsky.social labs! Happy to have played a tiny role in this important study.
www.cell.com/cell-reports...

Great opportunity for neuroscience postdocs!

SPiNES was such a great experience. Highly recommend!

Thank you, Priya! 🥰

Congratulations, Priyanka! Very exciting!

Microglial cGAS-STING-TBK1 activation in paraventricular thalamus mediates sleep and emotional disturbances in lupus mice www.sciencedirect.com/science/arti...

Thank you, @sarahnaguib.bsky.social! I'm gonna miss you 🙂

Thank you, Monica! Hope all is well.

Thank you, @mehdijorfi.bsky.social!

Huge thank you to my mentors @liganlab.bsky.social, @shuibingchen.bsky.social, @studerl.bsky.social and Shelley Berger for all the mentoring and support throughout my journey. Big shoutout to all present and past members of @liganlab.bsky.social for all their support along the way.

I am thrilled to announce that I will be starting my lab at
@washumedicine.bsky.social, Department of Pathology & Immunology as an Assistant Professor this month. The lab will study the role of innate immunity in neurodegeneration and brain aging. We'll be hiring at all levels. Details soon!

The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway The Christchurch mutation (R136S) in the APOE3 (E3S/S) gene is associated with attenuated tau load and cognitive decline despite the presence of a cau…

🚨Our new paper is out!🚨 We uncover a protective mechanism of the rare APOE3 Christchurch (R136S) mutation against tauopathy—by suppressing microglial cGAS–STING–interferon (IFN) pathway, a key inflammatory axis triggered by tau. www.sciencedirect.com/science/arti...

Congrats to @sarahnaguib.bsky.social, ‪@ertorres.bsky.social, @chloelopezlee.bsky.social et al!

The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway The APOE3 Christchurch mutation (R136S) reduces tau pathology despite the PSEN1 mutation and high amyloid, though its protective mechanism remains unclear. Naguib et al. show that R136S suppresses mic...

The new paper from the Gan lab out today in Immunity shows the Christchurch mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway. www.cell.com/immunity/ful...

The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway The APOE3 Christchurch mutation (R136S) reduces tau pathology despite the PSEN1 mutation and high amyloid, though its protective mechanism remains unclear. Naguib et al. show that R136S suppresses microglial cGAS-STING-IFN signaling in tauopathy mice. Inhibiting cGAS preserves synapses and mimics R136S-linked gene expression, suggesting that cGAS suppression is a key part of the underlying protective effects of R136S.

Online now: The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway

Our 12th Annual Appel Symposium was a huge success! Record attendance, insightful faculty speakers, and a vibrant poster session sparked meaningful conversations and highlighted the innovative research at WCM. A sincere thank you to all who attended and the WCM teams who made this event possible.

STING deletion protects against amyloid β–induced Alzheimer's disease pathogenesis INTRODUCTION While immune dysfunction has been increasingly linked to Alzheimer's disease (AD) progression, many major innate immune signaling molecules have yet to be explored in AD pathogenesis us...

STING deletion protects against amyloid β–induced Alzheimer's disease pathogenesis - Thanos - 2025 - Alzheimer's & Dementia - Wiley Online Library alz-journals.onlinelibrary.wiley.com/doi/10.1002/...

Contrary to Clear, Verifiable Facts, Secretary Kennedy Continues to Repeat Harmful Myths About Alzheimer’s and Dementia Research The Alzheimer's Association calls on HHS Secretary Kennedy to stop dangerous fabrications about the state of Alzheimer’s and dementia research.

www.alz.org/news/2025/ke...

Our fabulous group for #TargetAD25! We have had a wonderful 3 days so far of sharing insights, fostering collaborations, and driving progress toward understanding and treating Alzheimer’s disease💜
We can’t wait to celebrate with our gala dinner this evening! 😊💃

Excited to attend the #targetAD25 conference. Looking forward to all the great talks and discussions!
@fusionconf.bsky.social

Congratulations Celeste! 🥳