Yann
@LeGuenYann
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@Stanford_Neuro @stanford_qsu Deciphering the genetics causes of neurogenerative diseases.
Stanford, USA
Joined September 2012
I'm thrilled to share our new study out in @NatureMedicine! We show that a blood test can estimate how aged or youthful one’s organs are and that these organ ages predict future disease and lifespan. Final paper from my PhD in the @wysscoray lab. 🧵1/12 🔗
nature.com
Nature Medicine - In a large-scale proteomic study of biological aging of 11 organs from 44,498 individuals in the UK Biobank, the biological ages of the brain and immune system emerged as strong...
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A newly discovered biomarker in spinal fluid—the YWHAG:NPTX2 ratio—may indicate who will develop dementia and how quickly it will progress, according to a @NatureMedicine study led by @hammy_oh and senior author @wysscoray. https://t.co/mUS7Hl6Kpt
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In one of the largest genetic studies of its kind, Michael Greicius (@Stanford_Neuro), @LeGuenYann (#StanDOM) & team uncover the impact of rare genetic mutations that may be responsible for shortening lifespans, even in those who appear healthy.
medicine.stanford.edu
What if hidden genetic mutations could predict early death—even in healthy people? A Stanford study uncovers rare variants quietly shaping our lifespan.
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Another excellent and well-designed proteomics study with @hammy_oh, this time identifying a protein in CSF which is associated with cognitive impairments and predicts cognitive decline remarkably well
I am excited to present our new study out in @NatureMedicine where we discover a novel synaptic protein biomarker to predict if and when someone will get Alzheimer’s disease dementia. Part 2/3 from my PhD work in the @wysscoray lab. 🧵1/12 Full study 🔗:
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Our study’s implications thus extend beyond genetics, as they touch on the broader aspects of health care, public health policy, and preventive strategies against age-related diseases.
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Understanding the biological pathways through which these genes influence cancer and aging, as well as the environmental factors interacting with these pathways, will be essential for developing therapeutic targets aimed at extending a healthy lifespan.
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Our findings highlight the importance of understanding genetic factors driving the most prevalent causes of mortality at a population level, highlighting the potential of early genetic testing to identify germline & somatic variants increasing one’s susceptibility to cancer/aging
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Additionally, eight genes with pathogenic missense variants were associated with reduced lifespan (DNMT3A, SF3B1, TET2, PTEN, SOX21, TP53, SRSF2, RLIM). Many of these genes are involved in oncogenic pathways and clonal hematopoiesis.
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We found lifespan-associated loci (APOE, ZSCAN23) for common variants and six genes where burden of loss-of-function variants were linked to reduced lifespan (TET2, ATM, BRCA2, CKMT1B, BRCA1, ASXL1).
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Our UK Biobank study on the association of rare genetic variants with human lifespan is out today in Nature Communications! https://t.co/28oubjXSfU Strikingly, most of the genes we identified carrying lifespan-associated rare variants have been previously linked to cancer.
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Presenting our work on CHIP & AD today at #ASHG2024 @stanford_qsu Pass by poster 5035 if you’d like to hear more about this study
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At #ASHG2024 this week, message me if you are around and would like to meet. @stanford_qsu is looking for someone with hands-on spatial transcriptomics experience @GeneticsSociety
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Celebrating our neurology postdoctoral scholars during National Postdoc Appreciation Week #NPAW2024! Our faculty mentors know that postdocs are the backbone of innovation and progress and their dedication, knowledge, and creativity drive our research forward.
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For nearly 2 decades, Alzheimer’s disease (AD) “genome-wide” association studies only covered the autosomes. Today we unveil the X chromosome and prioritize SLC9A7, a.k.a. NHE7, as an AD risk gene. Article: https://t.co/lVybAmZWim Editorial: https://t.co/kAO2lS9PLq
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This X chromosome-wide association study of Alzheimer disease (AD) across 1,152,284 individuals identified SLC9A7 as a novel risk locus and provides initial insights into the role of X chromosome in sex-based differences in AD. https://t.co/LLty1ZdVgb
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At AAIC this week presenting some of my work on CHIP (clonal hematopoiesis) & AD @stanford_qsu @Stanford_Neuro . Pass by today at poster 783 to learn about somatic variants and potential caveats in replicating Bouzid et al. (2023, Nature Med)
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I'm excited to share 2 of our new studies now out as preprints on BioRxiv! https://t.co/7hswGUE7qc
https://t.co/Byk02tlVMq From @wysscoray lab in collaboration with many amazing groups including... 1/5
biorxiv.org
Rates of cognitive decline in Alzheimer’s disease (AD) are extremely heterogeneous, with ages of symptom onset ranging from age 40-100 years and conversion from mild cognitive impairment to AD...
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The UK Biobank (UKB) has been an amazing field changing resource for the past decade. Unfortunately, and very suddenly, they have decided that to work with their data you now *must* use their “Research Analysis Platform” (RAP). @uk_biobank I guess there have been general warning
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