Director NCI-designated Cancer Genome and Epigenetics Program at SBP, Co-Editor-in-Chief Aging Biology Journal, Road/Gravel/Mtn Cycling, Wolf Pack Cycling.
San Diego, CA
Joined August 2020
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New road bike. S-WORKS Tarmac SL7, Campy SR wireless and disc, Campy Bora Ultra WTO wheels👍 No excuses now😧
A conversation with my collaborator Joao Passos @MayoClinic about mitochondria and cell senescence mitoworld.org/mitochondria-a…
Great study from @ACovarrubiasPhD and team. In our recent paper on Cyclin D1 in senescence pubmed.ncbi.nlm.nih.gov/4262… we noted that Cyclin D2 was up in senescence. Anthony and team have figured out the function. Surprising new roles for both D1 and D2. See also work of @marc_dema
The p53-p21-Cyclin D2 regulatory axis drives metabolic reprogramming and a distinct senescent macrophage senotype during aging and MASLD
biorxiv.org/content/10.64898…
Could we have got here earlier if not such a focus on amyloid and tau as targets? ApoE has been telling us for years that cholesterol/lipid metabolism is important in Alzheimer’s
1/
Do you carry ApoE4? About 1 in 4 ppl do. 1 copy: ~3X Alzheimer's risk. 2 copies: ~10X.
On Sept 21, Europe approved obicetrapib, a cholesterol drug that, in a large trial, lowered multiple AD markers in ApoE4 carriers.
Yes, a drug engineered to prevent heart attacks seems to lower AD biomarkers.
Read on for details.
Great thread. This is very exciting, if it holds up and extends to cognition/disease prevention. Obicetrapib is one of the most exciting emerging new drugs.
1/
Do you carry ApoE4? About 1 in 4 ppl do. 1 copy: ~3X Alzheimer's risk. 2 copies: ~10X.
On Sept 21, Europe approved obicetrapib, a cholesterol drug that, in a large trial, lowered multiple AD markers in ApoE4 carriers.
Yes, a drug engineered to prevent heart attacks seems to lower AD biomarkers.
Read on for details.
Peter Adams🇪🇺🇺🇳 retweeted
🔥 We’re hiring! 🔥
My lab is seeking a postdoctoral fellow for studying the role of metabolic imbalance in aging, cancer and neurodegeneration @jobRxiv @mitojobs @ScienceCareers #hiring #metabolism #massspectrometry Join us!
Agree this is a great synthesis - and I think can likely be applied to other aging disease mechanisms in other tissues; for example, pathology caused by senescent cells, inflammation…….can also apply to interactions between multiple “hallmarks of aging”
A brilliant new @Nature synthesis of what we know about Alzheimer's disease pathogenesis, which is non-linear, with discrete phases (Figure), and notable inflection and transition points. Also helps to explain why symptoms do not correlate with underlying pathology.
nature.com/articles/s41586-0…
Peter Adams🇪🇺🇺🇳 retweeted
Nuclear export of R-loop by the DDX1 and XPO1 complex promotes senescence-associated secretory phenotype and inflammaging
nature.com/articles/s43587-0…
Peter Adams🇪🇺🇺🇳 retweeted
Tumors don’t evolve alone.
📣 New @GenomeBiology Collection on the Tumor Microenvironment: single-cell, spatial & multi-omic studies of how the TME shapes tumor evolution and therapy response.
Guest eds: @IamLinghua @kchenken & me
🗓️ until 19 May 2027
link.springer.com/collection…
Peter Adams🇪🇺🇺🇳 retweeted
🚨New preprint from the lab!🚨
LINE-1 (L1) #transposons become transcribed with #aging and #senescence, and are thought to contribute to #inflammaging. But what happens to a healthy, non-senescent human cell when #L1 turns on? biorxiv.org/content/10.64898… A 🧵, 1/7
@USCLeonardDavis
Excellent article, Alan! The focus on mutations in cancer and the difficulty of their early detection which you discuss has contributed to the focus on advanced cancers. But there are many causes of cancer in aging, not only mutations - so more opportunities for prevention.
Link to full piece: communitymorgue.com/p/the-fi…
Fascinating discussion with Julia Belk and my @sennetresearch colleague Nathan Zemke on age- dependent replacement of brain microglia. Consequences not clear to me though. Nathan et al seem to suggest detrimental, but Julia et al protective from Alzheimer’s. Both, perhaps?
Around age 50 your blood monocytes (Micro 2) begin a "hostile takeover" replacement of your brain microglia immune cells (Micro 1) and can promote inflammation. Two impressive studies made this remarkable discovery independently with different methods. In conversation with their lead authors, @juliabelk and Nathan Zemke erictopol.substack.com/p/two…
A paradoxical role for Cyclin D1 in senescent cells. Unexpected expression of CCND1 in senescent cells was shown decades ago. @AdarshRajesh5 and Boshi Wang (@marc_dema lab) showed pro-inflammatory function. nature.com/articles/s43587-0… nature.com/articles/s43587-0… nature.com/articles/s43587-0…
This looks like a great meeting!
Speakers also include Sir Tony Kouzarides, Coleen Murphy, Gio Silva Garcia, @senergystic, Ali Shilatifard, @AdamsBioAging @Yael_David__ Francois Fuks, and more! #Epigenetics #Aging
Michael Alcaraz, a very talented PhD student, led this study showing that NAMPT activation uncovers a senescence-specific vulnerability and promotes healthy aging in combination with NAM. Small molecule NAMPT activator to boost NAD+, identified at SBP. biorxiv.org/content/10.64898…
It has been a pleasure and privilege to contribute to SenNet for the last 4 years; to participate in a true collaborative effort to build a landmark resource that is changing the way we think about cell senescence. I'm excited to read this growing collection of articles.
✨The SenNet program aims to map and characterize senescent cells across age, tissue, and species. Discover research and opinion emerging from the SenNet project in a new cross-journal collection in the Nature portfolio ✨nature.com/immersive/s43587-…
ICSA Travel Awards now open! docs.google.com/forms/d/e/1F…
docs.google.com/forms/d/e/1F…
I’m pleased to share this new study in @Nature led by Joao Passos and Helene Martini @MayoClinic “Mitochondrial metabolism and epigenetic crosstalk drive SASP”. An integration of two of the many signals reported to drive SASP. rdcu.be/fwGTf
Interesting and inspiring…….Patrick Hsu: How Is AI Catalyzing Life Science? erictopol.substack.com/p/how…