I am very excited to be part of the study entitled “High prevalence of CNS-directed autoantibodies in patients with schizophrenia” which outlines the identification of many autoantibodies, including those targeting the BBB in schizophrenia patients.
https://t.co/80ZmrfqemW
Newly published work from our lab
showing changes in ribosome associated mRNA in chronic conditions of disturbed flow and circulating blood lipids, and regulation of this and CD8 T cell accumulation by Elavl1 :https://t.co/2DIuKdD5tY (follow us on bluesky : 1patrickmurphy)
Very interesting mouse model of preeclampsia - based on maternal, not fetal loss of KLF4 - where hypertension does not develop after gene deletion, but does with pregnancy: https://t.co/XHEyI1xmUA
A mouse model of Nose bleeding
#HereditaryHemorrhagicTelangiectasia#HHT
Bmx+ Endothelial Cell ALK1 KO🐭
Recurring epistaxis
Multifocal cerebral microhemorrhage
Arterial tortuosity, ectasia
Arteriolar smooth muscle cell wrapping defects
Loss of arterial identity (⏬Ephrin B2)
⏬pial or mesenteric arterial tone
Rupture of arteriolar or capillary beds?😁
@mf_navedo@Rong_A_Wang@CircRes 2026
https://t.co/RRNGrS2LLu
Considerations in the Use of Mouse Models of Vascular and Valvular Calcification
Our new article is now published @atvbahajournals
@YinTintut @UCLAHealth https://t.co/uiQJGs0olG
🩸 🧠 ⏱️ What if a blood test could predict WHEN an individual would develop symptoms of Alzheimer’s disease? High plasma p-tau217 predicts greater risk for Alzheimer’s symptoms—do the plasma p-tau217 levels provide insights into WHEN symptoms might begin?
We found that after a certain level, plasma p-tau217 increased consistently across individuals and allowed creation of “clock” models that could be used to estimate age at p-tau217 abnormality (https://t.co/7v2DppCh4i). The age at p-tau217 abnormality was strongly associated with the age that Alzheimer’s symptoms began. Interestingly, older individuals developed symptoms more quickly after p-tau217 abnormality.
These models are not yet accurate enough to be useful to individuals, but we expect they can be improved by adding additional blood biomarkers and clinical features. We have created an application to view the results (https://t.co/p7P4h0z0zX) and shared all our code to accelerate progress. The eventual goal is to help individuals to understand their likelihood of developing Alzheimer’s symptoms.
@KellenPetersen@FNIH_Org@WashUNeurology@alzassociation #ENDALZ
We are excited to share a new discovery in heart transplant https://t.co/zht8cCwhFB , which shows a critical role for the endothelium in organizing long term immune responses and cardiac allograft vasculopathy.
Noor can, and it was an amazing and inspirational learning experience to hear about her work. Thanks for your visit, and best of luck in continuing to develop your exciting and powerful delivery system to cancer matrix. Only afterwards did I realize I forgot to get a photo!
It was pleasure to host my former lab mate @N_Jailkhani from MatrisomeBio yesterday at @uconnhealth. Not many can say that they both developed a new technology hands on, and then led this into the market as the CEO of a successful company.
A postdoc position is open in the @AgalliuLab for a scientist with a strong PhD background in Neuroscience, Neuroimmunology or Vascular Biology and interest in neurovascular / BBdysfunction in CNS disorders. Please contact me with your CV and cover letter if you are interested.
@DAgalliu Interesting and slightly different from healthy aged brain ECs- where although a signature for ISGs appears, the top p65 associated genes are heaviest for matrix and cell-junctions, maybe due to the degree of other cytokine stimulation in stroke (high) vs aging (low)?
am excited to share with everyone a new pre-print of the work of a very talented MSTP student Mary Claire Tuohy entitled “Endothelial Type I Interferon signaling modulates the vascular response to ischemic brain injury”.
https://t.co/QFv65MxccM
Interesting new work - modeling NFkB dysfunction in the micro vasculature in AD in vitro. Could be interesting to see to what extent this is determined by loss of TDP-43 in the endothelial cells as we observed by inCITE-seq : https://t.co/ANLcFRhcYs and https://t.co/SVPWVLzWFM
URGENT: A leaked HHS memo proposes cutting all funding to the National #ALS Registry. This would erase decades of critical research & let down 20,000+ who've contributed. We’re calling on Congress to stop this NOW.
Read our letter and take action today: https://t.co/nQ2zC5eF8i
Despite strong headwinds our work continues. @CheemalaAshok shows that even a single point mutation in TDP-43 leads to large defects in cell-cell junction and barrier, and that brain endothelial deletion disrupts the BBB and leads to FTD-like behavior https://t.co/SVPWVLzWFM
Congratulations to Ashok, an exceptionally talented scientist who would be a tremendous junior faculty hire. Thank you to our collaborators @jacksonlab, lab members including @omaruximab and as others not on this platform, including Riqiang Yan.