Exciting to see this modern genomic approach to classification of psychiatric disorders! Hopefully this will eventually lead to potential new gene therapy targets for treatment.
Analysis of more than one million people shows that mental-health disorders fall into five clusters, each of them linked to a specific set of genetic variants.
RCT: Smartphone-based ecological momentary assessment found greater morning fatigue but reduced afternoon and evening fatigue in patients with Insomnia treated with suvorexant vs placebo.
Question What is the effect of insomnia suvorexant pharmacotherapy on daytime insomnia symptoms as assessed via smartphone ecological momentary assessment (EMA)?
Findings In this randomized clinical trial that included 40 older adults with insomnia, traditional outcomes assessments detected differences between suvorexant and placebo groups in daytime insomnia symptoms; however, EMA was sensitive to detect effects of insomnia pharmacotherapy at various times of day.
Meaning These findings suggest that EMA warrants further refinement in sleep and psychiatric research and clinical care.
A new study reveals how viruses that infect bacteria, called bacteriophages or “phages,” use a tiny piece of genetic material to hijack bacterial cells and make more copies of themselves.
The research shows that a very small RNA molecule, called PreS, acts like a hidden “switch” inside the bacterial cell. By flipping this switch, the virus can change how the bacterial cell works and push the infection forward.
Until now, most phage research has focused on viral proteins. This study shows that phages also use RNA molecules to quickly reprogram the host cell after the bacterial genes have already been read and bacterial messages (mRNAs) were made, adding an extra layer of control during infection.
PreS attaches to these important bacterial messages and tweaks them in a way that helps the virus copy its DNA and move more efficiently toward the stage where new viruses are produced and burst out of the cell, killing the bacterium.
Using advanced methods to map RNA–RNA interactions (termed RIL-seq), the researchers found that one of PreS’s key targets is a bacterial message that makes DnaN, a protein that plays a central role in copying DNA. By helping the cell make more DnaN, PreS gives the virus a strong head start in the infection process.
Interestingly, PreS works by changing the shape of the bacterial dnaN message.
Normally, part of this message is tightly folded, which makes it hard for the cell’s protein-making machines (ribosomes) to access. PreS binds to this folded region, opens it up, and allows ribosomes to read and translate the message more efficiently.
A great paper where Miyakawa et al. show attenuation of seizures using chemogenetics for the first time in a nonhuman primate model of epilepsy. I hope chemogenetics moves into clinical trials soon (this paper was published in 2023), it seems very promising as a therapeutic modality. [ https://www.nature.com/articles/s41467-023-36642-6](https://www.nature.com/articles/s41467-023-36642-6)
Pharmacological and surgical treatments of epilepsy can have unsatisfactory outcomes, so a more targeted and on-demand approach is desirable. Here, the authors demonstrate the usage of inhibitory chemogenetics in male nonhuman primates to attenuate the magnitude and spread of cortical seizures and subsequent body convulsions.
Lower handgrip strength is associated with higher 2-year death risk in older heart failure patients, with stronger impact at advanced ages. @NakadeTaisuke @yuya_matsue
Astrocytic lipid metabolism in brain signaling.
Glia previously thought to be support cells of brain but recent evidence suggest that the astrocytes, the most abundant glial cell type in addition to supplying neurons with lactate via glycolysis also actively engage in lipid metabolism, especially mitochondrial fatty acid β-oxidation.
Researchers in this review integrate astrocytic fatty acid ß-oxidation and ketogenesis, alongside other metabolic pathways converging on reactive oxygen species dynamics, including cholesterol metabolism and peroxisomal β-oxidation.
Thus, convergence of energy metabolism to signaling may provide new insights to central nervous system function and dysfunction. https://sciencemission.com/astrocytic-lipid-metabolism
Astrocytes, the most abundant glial cell type in the central nervous system, have traditionally been viewed from the perspective of metabolic support, particularly supplying neurons with lactate via glycolysis. This view has focused heavily on glucose metabolism as the primary mode of sustaining neuronal function. However, recent research challenges this paradigm by positioning astrocytes as dynamic metabolic hubs that actively engage in lipid metabolism, especially mitochondrial fatty acid β-oxidation. Far from serving solely as an energy source, fatty acid ß-oxidation in astrocytes orchestrates reactive oxygen species-mediated signaling pathways that modulate neuron-glia communication and cognitive outcomes.
The first NMNH human trial shows NAD+ levels increased up to 3x in 90 days. Here’s what the data actually reveal—and what’s still missing.
Some links are affiliate links so we will earn a commission when they are used to purchase products.
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Qualia (15% off: MODERN) https://bit.ly/4jlaibe, Senolytic.
Wellness Extract (10% off: MODERNWE) http://wellnessextract.com/RICHARDWE Geranylgeraniol • Vit E
AX3 Life (20% off: MODERN20) https://tinyurl.com/2t3w26nw — Astaxanthin.
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The first human clinical trial results for NMNH are here. In this 90-day randomized, double-blind, placebo-controlled study, NMNH increased NAD+ levels up to 3x in healthy adults, with participants reporting improvements in energy and fatigue. But before you get too excited, there are important limitations to understand.
In this video, I break down the trial design, explain what the NAD+ increases actually mean, review the subjective outcomes like energy and emotional well-being (measured via SF-36), and discuss why the biological age claims are difficult to interpret. I also cover safety data and what we still need to know.
This is promising early data for NMNH vs NMN, but it’s unpublished, lacks key details, and needs independent replication. Here’s everything you need to know about what this trial does and doesn’t tell us.
Key topics: NMNH clinical trial, NAD+ boosters, NMN vs NMNH, longevity supplements, anti-aging research, NAD+ levels, UthPeak study, Phase I trial results.
📚 Chapters.
0:00 — Introduction & Trial Overview What this video covers and the trial basics.
1:39 — Trial Design & Methodology Study structure, participants, and objectives.
2:31 — NAD+ Results The primary outcome: dose-dependent increases.
3:18 — Subjective Outcomes & Limitations Energy, mood, biological age claims, and why interpretation is difficult.
6:26 — Safety & Final Thoughts Tolerability data and what comes next.
🌐Links in this video.
NMNH Clinical Trial https://www.clinicaltrials.gov/study/.… nicotinamide mononucleotide is a new and potent NAD+ precursor in mammalian cells and mice https://faseb.onlinelibrary.wiley.com… Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+ and Suppresses Glycolysis, the TCA Cycle, and Cell Growth https://pubmed.ncbi.nlm.nih.gov/33793… *************************************** Health claims Disclosure: Information provided on this video is not a substitute for direct, individual medical treatment or advice. Please consult with your doctor first. Products or services mentioned in this video are not a recommendation. Audio Copyright Disclaimer Please note that we have full authorization to the music that we used in our videos as they were created using the service WeVideo which provides the rights to the music. The rights are detailed in the terms of use that can be reviewed here https://www.wevideo.com/terms-of-use and any following inquiries should be addressed to [email protected]. ********************************************** #nmnh #nad #nmn.
Reduced nicotinamide mononucleotide is a new and potent NAD+ precursor in mammalian cells and mice.
https://faseb.onlinelibrary.wiley.com…
Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+ and Suppresses Glycolysis, the TCA Cycle, and Cell Growth.
https://pubmed.ncbi.nlm.nih.gov/33793…
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A rebrand for proteasome inhibition in solid tumors.
In this Research Letter, Jonathan M. Hernandez & team investigate the potential of hepatic artery infusion pump delivery of carfilzomib, to continuously direct a large dose to the tumor with least hepatic toxicity.
Address correspondence to: Jonathan M. Hernandez, National Cancer Institute, NIH, 10 Center Drive, Room 4W-3752, Bethesda, Maryland, 20,892, USA. Email: Jonathan. [email protected].
Burkitt’s lymphoma is a rare and aggressive blood cancer characterized by a translocation of the MYC gene. It occurs most often in children and young adults. In recent years, CAR-T cell therapy—often referred to as a “living drug” and administered as a single dose—has been approved for certain types of blood cancer, offering hope for a cure even in severe cases. However, its effectiveness against Burkitt’s lymphoma has been limited. Moreover, developing drugs that directly target MYC—the root cause of this cancer—has proven challenging for decades.
Recently, a study led by Dr. Hiroshi Kotani, Assistant Professor at Kanazawa University in collaboration with a scientist at Roswell Park Comprehensive Cancer Center in Buffalo, NY, U.S., revealed that a SUMOylation inhibitor can suppress MYC activity. Building on this finding, the research team investigated whether combining CAR-T therapy with the SUMOylation inhibitor TAK-981 could improve outcomes for Burkitt’s lymphoma. The research is published in Signal Transduction and Targeted Therapy.
The team first confirmed that the SUMOylation inhibitor effectively slowed the growth of Burkitt’s lymphoma cells and altered their signaling pathways. They then examined the inhibitor’s effect on CAR-T cells and discovered a dual role: While it initially activated the CAR-T cells in a way that could hinder long-term effectiveness, it also triggered a built-in “safety brake” mechanism. These insights suggested that using only a limited dose of the inhibitor could maximize the benefits of CAR-T therapy as a durable, living treatment.