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Polyamine metabolism as a regulator of cellular and organismal aging

Polyamines — putrescine, spermidine, and spermine — are ubiquitous cationic molecules that are essential for cellular proliferation and homeostasis. Their intracellular concentrations decline with age, contributing to physiological and cognitive deterioration. Recent studies have revealed that spermidine supplementation extends lifespan and improves cognitive and cardiac function in various model organisms, suggesting that maintaining polyamine balance has anti-aging potential. Polyamine metabolism is tightly regulated through biosynthesis, degradation, and transport; however, age-associated upregulation of spermine oxidase (SMOX) and accumulation of its toxic byproduct acrolein promote oxidative damage and cellular senescence. Suppressing SMOX activity or polyamine degradation attenuates senescence markers and DNA damage, highlighting spermine catabolism as a therapeutic target. Polyamines also modulate epigenetic regulation, including DNA methylation and histone acetylation, thereby influencing gene expression and chromatin structure during aging. Moreover, polyamine-dependent hypusination of eIF5A sustains protein synthesis in senescent cells. These multifaceted actions indicate that polyamine metabolism integrates redox control, translational regulation, epigenetic maintenance and autophagy to determine cellular and organismal longevity. While animal studies demonstrate clear anti-aging effects of spermidine and spermine, human clinical evidence remains limited, with variable outcomes likely due to bioavailability and metabolic conversion. Future strategies combining dietary or probiotic polyamine enhancement, enzyme-targeted inhibitors, and personalized metabolic interventions hold promise for extending healthspan. Collectively, maintaining optimal polyamine homeostasis emerges as a key approach to counteract aging and age-related diseases.

SGLT2 Inhibitors for Nondiabetic Heart Failure: Equipping PCPs for Success

Once diabetes drugs, SGLT2 inhibitors are now key therapies for heart failure—even in patients without diabetes. A new primary-care guide reviews indications, benefits, and practical prescribing tips to help clinicians integrate these agents into routine HF care.

Are PCPs ready to adopt SGLT2 inhibitors beyond diabetes?

While proven to help, primary care clinicians have been slow to use the drugs once considered only for patients with diabetes.

Role of Dopamine in Pain

Dopamine is a member of a class of molecules called the catecholamines, which serve as neurotransmitters and hormones. In the brain, dopamine serves as a neurotransmitter and is released from nerve cells to send signals to other nerves. Outside of the nervous system, it acts as a local chemical messenger in several parts of the body.

Image Copyright: Meletios, Image ID: 71,648,629 via shutterstock.com

A number of important neurodegenerative diseases are associated with abnormal function of the dopamine system and some of the main medications used to treat those illnesses work by changing the effects of dopamine. The condition Parkinson’s disease is caused by a loss of dopamine secreting cells in a brain area called the substantia nigra.

Using Blender In Real-World Cosmology Research

We recently shared the story of Blender’s role in the adult animated series Il Baracchino, and now, a fascinating new article by Ph.D. student MohammadHossein Jamshidi showcases how he applied Geometry Nodes in his cosmology research.

Cosmology is the study of the universe and its fundamental nature. MohammadHossein Jamshidi, from Shahid Beheshti University in Iran, has also worked as an animation engineer in the game industry since 2012. His initial inspiration to apply Blender to scientific work came from the creative projects of Seanterelle, which led him to experiment with using Geometry Nodes for cosmological computations.

In the article, he shares several ideas and techniques for using Blender in his research, and he believes that these approaches could be applied to other areas of science as well. All the files featured are freely available on this GitHub repository.

Grant supports research into how microglia may spread toxic tau in Alzheimer’s

A paper describing Hopp’s upcoming study published on the CureAlz website, titled, “How Do Microglia Contribute to the Spread of Tau Pathology in Alzheimer’s Disease?”, says that while tau aggregates are a defining feature of Alzheimer’s disease and closely track with brain cell loss, memory problems and cognitive decline, much still isn’t known about how it spreads or what role the brain’s immune system plays in the process.

There is evidence, it says, that toxic forms of tau, which have become “misfolded” or dysfunctional, act like a “bad influence.”

“When they encounter nearby healthy tau proteins, they cause them to misfold as well, triggering a chain reaction that spreads from one brain region to another,” according to the paper. “Microglia … are among the first to encounter these toxic tau ‘seeds.’ Normally, microglia protect the brain by clearing debris and helping repair damage. But growing evidence suggests that microglia may also contribute to tau’s spread by engulfing misfolded tau and inadvertently releasing it, thereby amplifying its harmful effects.”

A researcher with the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio has received a two-year, $402,500 grant award from the Cure Alzheimer’s Fund to study how microglia, the brain’s resident immune cells, paradoxically might contribute to the spread of toxic forms of tau protein in the disease.

Sarah C. Hopp, PhD, associate professor of pharmacology with the Biggs Institute and the South Texas Alzheimer’s Disease Research Center, along with her lab have been instrumental in uncovering the behavior of microglia. UT Health San Antonio is the academic health center of The University of Texas at San Antonio.

Starting this month, Hopp’s lab will test the hypothesis that microglial uptake of tau is a key mechanism driving its spread through the brain, and that specific molecular pathways determine whether this process protects or harms neurons. The Cure Alzheimer’s Fund, also known as CureAlz, is a nonprofit organization that funds research “with the highest probability of preventing, slowing or reversing Alzheimer’s disease.”

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