@AsmaaNamoos Some of my family members live in the city ! Enjoy your stay
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Imad Damaj
2K posts
Imad Damaj
@DamajLab
VCU Pain And neuropathy Research Program Neuropharmacology of drug addiction and pain- nicotinic Lab
Virginia, USA انضم Haziran 2015
331 يتبع581 المتابعون
@wickedneuro @DrJKhokhar Yep! Time to include nutrition in your studies Ryan !
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Our latest paper on Aromatase inhibitors induce pain-like musculoskeletal symptoms!
bpspubs.onlinelibrary.wiley.com/doi/10.1111/bp…
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@sushmajumdarlab Cool! Hopefully that will lead to the development of new ligands !
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Join us for this month's Dean's Select Lecture @IcahnMountSinai when Dean Emeritus Dennis Charney will discuss the therapeutic potential of psychedelic drugs. November 3 in Davis Auditorium at 4 pm.
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@brainaddiction The outcome measure is little bit odd. Is that common in these small clinical studies ?
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Impressive results on alcohol drinking (and smoking) replicating preclinical, epidemiological and observational data. Very likely that GLP1s agonist will become the first medication that is effective to treat all addictions.
JAMA Psychiatry@JAMAPsych
Low-dose semaglutide reduced alcohol craving and consumption in adults with alcohol use disorder. ja.ma/4gQUxaM
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@DrJoyceDaSilva @UMMedNeuro @UMBaltimore @NIHPainResearch @NIH @NIHFunding Congratulations! Well deserved!
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It’s official. 🎉Grateful to receive NIH funding for two R01s: one as Sole PI and another in collaboration with UCSD. Thank you to my career mentors and team for their continued support and guidance.
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@hubermanlab @StanfordPain academic.oup.com/jnci/article/1…
Acetyl-L-Carnitine worsened neuropathy induced by chemotherapy!
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OTC Supplements for pain. For MDs & scientists out there that are supplement averse, be aware this is @StanfordPain
= Times are changing! In fact, they have changed. The most knowledgeable MDs are embracing the full kit as useful: behaviors, supplements, Rx Meds & mindset.
Stanford Pain Medicine@StanfordPain
Supplements and chronic pain: What does the research say? A list of 5 supplements that may help with nerve and chronic pain, as part of a broader treatment plan: 1. Acetyl-L-Carnitine -Helps your cells make energy. - Studied in people with diabetic nerve pain. - May help nerves send signals better. 2. Alpha Lipoic Acid - Works as an antioxidant and affects calcium in cells. - May help with nerve pain. - Can cause an upset stomach in some people. 3. Vitamin C - Not just for colds. -Some research shows it may lower the chance of nerve pain after surgery. 4. Fish Oil (Omega-3s) - May help reduce inflammation and pain. - But it can make your blood thinner, which might raise the risk of bleeding. 5. Creatine - Often used by athletes for muscle strength. - Small studies suggest it might help people with fibromyalgia and similar conditions.
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A beautiful paper from the Waxman group!
Nav1.8: Intrinsic limits on the functional effect of abrogation in DRG neurons | PNAS pnas.org/doi/10.1073/pn…
“Some nociceptors are weakly affected by Nav1.8 subtraction, suggesting other channels may need targeting for full relief.”
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@FlyBottleEscape No doubt that the work is fantastic and advance our understanding of pain. Hopefully more work will be coming from them on it!
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@DamajLab i still like the paper overall ... but since they do these assays all the time, im skeptical they didnt try a chronic pain model, which makes me think there was no effect on thermal hypersensitivity or other measures
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Noted by Rev 1 in the Peer Review file (comment + author response below), the mouse tested for acute sensory effects is a global knockout for SLC45A4
the paper claims DRG as the locus for the GWAS/behavior impacts on pain
SLC45A4gene is found in near every cell in the🐭brain
Veera Rajagopal @doctorveera
This is a cool paper, but not sure if the findings are impressive enough to be too excited about. The authors used a GWAS of a pain phenotype and decided to study a gene (SLC45A4) at a specific locus in detail. The genetic association itself is robust, replicates across multiple cohorts, but not clear if SLC45A4 is the causal gene. Despite the availability of rare variants in UK Biobank, no mention of SLC45A4 coding variant associations with pain. Quick look at the genebass, shows nothing striking for pain. Being the closest gene and not well characterized before, the authors studied the gene in detail using a range of functional experiments. In the process, they discovered that the gene encodes a polyamine membrane transporter and expressed in dorsal root ganglion (DRG) neurons, among others. They went on to create a knockout mouse. The phenotypes in the knockout seem to be similar to the wild type for the most part: - Anatomically and histologically, no differences. - Biochemically, there were differences in the polyamine levels in the spinal cord, DRG and plasma, which validates Slc45a4 as a polyamine transporter. - Behaviorally, no remarkable differences in sensory phenotypes, except for reduced sensitivity to thermal and chemical-induced pain in KO mice. Here is one critical, puzzling observation: the missense variant (p.Asn718Asp) in SLC45A4 (believed to be the causal variant) has no impact on the polyamine transport when recreated in the. Not only that, mutating the site to any other amino acid (Ala, Arg, Trp) had no impact on polyamine transport. Overall, the genetic association in humans and KO phenotypes in mice are interesting on their own, but no convincing connection between the two. Genetic targets for pain have been extraordinarily difficult as exemplified by recent setback by Vertex's Nav1.8 (SCN10A) inhibitors, which produced unimpressive results in clinical trials. This is despite that SCN10A had a strong human genetic association with pain (both common and rare variants). So, I'm not sure if SLC45A4 could be considered a promising drug target for pain yet. Maybe it is, but we can't say that with the current evidence. Middleton, Markússon, Newstead, Bennett, et al. Nature 2025 nature.com/articles/s4158…
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@FlyBottleEscape I agree Greg. I was wondering the same since the group does chronic pain models. It would have been nice to do also some spontaneous pain testing also
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Taking 2+ years to make a KO mouse to then not test them in a chronic pain model is odd; this would take a week to CFA or 3 weeks to SNI
Since the human GWAS was results are from chronic pain patients seems like a reasonable thing to have done
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Just out in @TheJournal_Pain:
“Paclitaxel-Induced Neuroinflammation After Systemic Administration in Male and Female Mice”
Paclitaxel-induced increase in neuroinflammation is time-, sex-, and tissue- dependent.
jpain.org/article/S1526-…
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Our latest on adolescent nicotine “Adolescent nicotine exposure affects later-life nicotine reward and withdrawal in mice” with the talented graduate student @BuzziBelle
sciencedirect.com/science/articl…
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abstract deadline has been extended for the 10th annual NIDA-sponsored CPDA conference (Chemistry & Pharmacology of Drug Abuse) here at Northeastern University in Boston, 8/7-8/8. It is a fantastic meeting, hope to see you there! cpdaconference.org
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@DrJoyceDaSilva @UMMedNeuro Thank you Joyce! An awesome visit to a great group of pain scientists and very interesting research! Looking forward to some great collaborations in the future!
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Honored to host Dr. Damaj @DamajLab at UMB today! Great talk on exciting new data and a wonderful opportunity to connect. Looking forward to potential collaborations🤩. Quick lunch pic📸 @UMMedNeuro
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‼️New and timely publication about the validity of animal models
Tran et al. optimized an alcohol abstinence model using naltrexone and varenicline, medications for people with AUD, highlighting the model's validity and potential use to identify new treatments.
10.1111/acer.70057
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