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Signaling roles for astrocytic lipid metabolism in brain function

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.

NMNH Triples NAD+ in First Human Trial: Here’s What That Means

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.

If you would like to support our channel please consider joining our patreon / modernhealthspan.
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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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Continue reading “NMNH Triples NAD+ in First Human Trial: Here’s What That Means” | >

Inhibition of 15-hydroxy prostaglandin dehydrogenase promotes cartilage regeneration

Aging or injury to the joints can lead to cartilage degeneration and osteoarthritis (OA), for which there are limited effective treatments. We found that expression of 15-hydroxy prostaglandin dehydrogenase (15-PGDH) is increased in the articular cartilage of aged or injured mice. Both systemic and local inhibition of 15-PGDH with a small molecule inhibitor (PGDHi) led to regeneration of articular cartilage and reduction in OA-associated pain. Using single cell RNA-sequencing and multiplexed immunofluorescence imaging of cartilage, we identified the major chondrocyte subpopulations. Inhibition of 15-PGDH decreased hypertrophic-like chondrocytes expressing 15-PGDH and increased extracellular matrix-synthesizing articular chondrocytes. Cartilage regeneration appears to occur through gene expression changes in pre-existing chondrocytes, rather than stem or progenitor cell proliferation.

Carfilzomib via HAI

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].

Clearing the brain of aging cells could aid epilepsy and reduce seizures

Temporal lobe epilepsy, which results in recurring seizures and cognitive dysfunction, is associated with premature aging of brain cells.

A new study by researchers at Georgetown University Medical Center found that this form of epilepsy can be treated in mice by either genetically or pharmaceutically eradicating the aging cells, thereby improving memory and reducing seizures as well as protecting some animals from developing epilepsy.

The study appears in the journal Annals of Neurology.

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