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Gardenias are known for their rich, earthy fragrance, waxy petals and brilliant white color that contrasts with the deep emerald green of their leaves. The plant has long been prized by herbalists, seekers of food and fabric dyes, and even pharmaceutical companies.

Now, a collaborative team of scientists at several research centers in the United States has found that a compound known as genipin, derived from the gardenia plant called Cape jasmine, can prompt nerve regeneration. Neurons damaged and stunted by disease find new life in the lab when exposed to the plant-derived compound.

The chemical comes from the fruit of this extraordinarily versatile plant. Gardenia shrubs, in general, are native to tropical and subtropical regions of Asia. But the plants are propagated globally by horticulturists and amateur gardeners who are most familiar with the flower’s beauty and the intoxicating scent of their perfume.

Years before tau tangles show up in brain scans of patients with Alzheimer’s disease, a biomarker test developed at the University of Pittsburgh School of Medicine can detect small amounts of the clumping-prone tau protein and its misfolded pathological forms that litter the brain, cerebrospinal fluid and potentially blood, new research published today in Nature Medicine suggests.

The biomarker test correlates with the severity of cognitive decline, independent of other factors, including brain amyloid deposition, thereby opening doors for early-stage disease diagnosis and intervention.

Since amyloid-beta pathology often precedes tau abnormalities in Alzheimer’s disease, most biomarker efforts have focused on early detection of amyloid-beta changes. However, the clumping of tau protein into well-ordered structures referred to by pathologists as “” is a more defining event for Alzheimer’s disease as it is more strongly associated with the cognitive changes seen in affected people.

As temperatures drop, norovirus cases increase and more of its RNA ends up in sewage. This year, wastewater samples in the United States show norovirus levels have already passed the previous two seasonal peaks.


The “Ferrari of viruses” is having a banner season. Norovirus, which races through cruise ships, homes, and long-term care facilities, is experiencing a remarkable winter surge in the Northern Hemisphere, sending large numbers of people racing to the bathroom and many others to the hospital, and in rare cases, proving fatal. In the United States, for example, 91 outbreaks of the intestinal virus occurred in the first week of December 2024, far above the previous maximum, 65, for the same week between 2010 and 2024. And levels of its genes in U.S. wastewater are an order of magnitude above last year.

“The early data for the early part of the season is certainly supporting that we’re going to have a pretty intense norovirus year,” says Lisa Lindesmith, who studies the virus at the University of North Carolina (UNC) at Chapel Hill. Some of the surge may be due to a new variant of the virus, unfamiliar to many people’s immune systems, and the resumption of cruises and other gatherings that the COVID-19 pandemic interrupted. And there’s no vaccine anywhere in sight: The most advanced candidate just failed a key trial and others won’t be ready for several years.

Norovirus thrives in cold climes, causing explosive diarrhea and vomiting that typically only last for a day. But several weeks after people recover, they can still shed the virus, and it can remain infectious for long periods on surfaces. It’s notoriously resistant to many disinfectants, and studies in adult volunteers have shown just a trace of virus is enough to sicken a person. Oysters are also a source of infection, because the filter-feeding mollusks concentrate the virus from contaminated water in their tissues. U.S. health officials issued several warnings about infected oysters in December, and France has banned oyster harvesting in certain regions because of norovirus outbreaks.

The interaction between cellular senescence and cancer is complex and multifaceted, senescence can both promote and inhibit tumor progression through various mechanisms. M6A methylation modification regulates the aging process of cells and tissues by modulating senescence-related genes. In this review, we comprehensively discuss the characteristics of cellular senescence, the signaling pathways regulating senescence, the biomarkers of senescence, and the mechanisms of anti-senescence drugs. Notably, this review also delves into the complex interactions between senescence and cancer, emphasizing the dual role of the senescent microenvironment in tumor initiation, progression, and treatment. Finally, we thoroughly explore the function and mechanism of m6A methylation modification in cellular senescence, revealing its critical role in regulating gene expression and maintaining cellular homeostasis. In conclusion, this review provides a comprehensive perspective on the molecular mechanisms and biological significance of cellular senescence and offers new insights for the development of anti-senescence strategies.

Cellular senescence is a complex and multifaceted biological process characterized by a stable arrest of the cell cycle in response to various stressors, such as DNA damage, oxidative stress, and oncogene activation (1). Although senescent cells no longer proliferate, they remain metabolically active and exhibit distinct phenotypic changes, including the secretion of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP) (2, 3). Senescence plays dual roles in physiological and pathological contexts: it is essential for processes like tissue remodeling, wound healing, and tumor suppression, yet its accumulation contributes to aging, chronic inflammation, and the progression of age-related diseases, including cancer and neurodegenerative disorders (4). Understanding the mechanisms underlying cellular senescence is crucial for developing therapeutic strategies to harness its beneficial aspects while mitigating its detrimental effects.

Scientists have provided a diagnosis for more than 500 European patients who did not know their condition. This work, which was performed by the Solving the Unsolved Rare Diseases (Solve-RD) consortium and was highly collaborative, has been reported in Nature Medicine.

In the European Union, a rare disorder is defined as one that occurs in fewer than five of 10,000 people. Genetic mutations are the cause of most of these rare disorders, but genetic sequencing cannot always provide an easy answer.

When cancer is detected earlier, it can improve outcomes for patients. Liquid biopsies are one way to improve cancer detection; these tests can analyze DNA in blood samples, which can reveal the presence of tumors because of circulating tumor DNA (ctDNA). Usually, genetic sequencing is used to assess this DNA, but that usually only identifies some types of cancers. Scientists have now created a new blood test called TriOx, which can analyze ctDNA in multiple ways and detect six types of cancer. The work has been reported in Nature Communications.

Usually, the analysis of ctDNA only focuses on one feature of the genome such as small variations in the DNA sequence that can reveal cancer, but TriOx uses an advanced tool called whole-genome TAPS (TET-Assisted Pyridine Borane Sequencing), which was combined with machine learning. This technique can analyze genetic as well as epigenetic features of DNA, like methylation.

Per-and polyfluoroalkyl substances (PFAS) are industrial chemicals used in the manufacturing of thousands of products, including cosmetics, carpeting, non-stick cookware, stain-resistant fabrics, firefighting foams, food packaging, and waterproof clothing.

They’re everywhere — the environment, our food, and even in our bodies. Peer-reviewed studies have shown that exposure to PFAS may lead to decreased fertility, developmental delays in children, and increased risk of some cancers. And they take hundreds or even thousands of years to break down.

For roughly the past 10 years, researchers have been looking for ways to remove PFAS from the environment or at least degrade them into harmless, inorganic compounds.

A study confirms the positive effects of exercise on insulinInsulin is a hormone produced by the pancreas, crucial for regulating blood glucose levels. It helps cells in the body absorb glucose from the bloodstream and convert it into energy or store it for future use. Insulin production and action are essential for maintaining stable blood sugar levels. In people with diabetes, the body either does not produce enough insulin (Type 1 diabetes) or cannot effectively use the insulin it does produce (Type 2 diabetes), leading to elevated levels of glucose in the blood. This can cause various health complications over time, including heart disease, kidney damage, and nerve dysfunction. Insulin therapy, where insulin is administered through injections or an insulin pump, is a common treatment for managing diabetes, particularly Type 1. The discovery of insulin in 1921 by Frederick Banting and Charles Best was a landmark in medical science, transforming diabetes from a fatal disease to a manageable condition. tabindex=0 insulin signaling proteins in the brain.