Phagocytosis – eliminating millions of dead cells every day – requires specialized cells such as macrophages, the true professionals, which migrate to engulf waste and dying cells. But they are not the only ones that can perform this task, as scientists at Howard Hughes Medical Institute (HHMI) discovered when they investigated hair follicle stem cells (HFSCs), a tissue in constant regeneration, to clarify how dying cells are detected and cleared in the epithelium and the mesenchyme.

People with the rare inherited metabolic disorder Gaucher disease have a deficiency in the lipid-digesting glucocerebrosidase enzyme, which causes the accumulation of harmful levels of glucolipids in various organs. The enzyme has a very short half-life, which rules out enzyme replacement as an effective therapy, and as things stand, there are few treatments for this and other lysosomal storage diseases (LSDs). Now, researchers have discovered two small molecules that enhance the activity of glucocerebrosidase in cellular models of LSD, pointing to a potential new approach to treating these diseases.

Researchers at the Walter and Eliza Hall Institute of Medical Research (WEHI) in Melbourne have discovered new cells that drive the aging process in the thymus that could unlock a way to restore function and prevent immunity from waning as we age. The thymus is the first organ in the body to shrink as people age. As this happens, the T-cell growth areas in the thymus are replaced with fatty tissue, diminishing T-cell production and contributing to a weakened immune system.

Scientists at Harvard Medical School have shown that in mice lacking amyloid beta (Aβ), the fundamental hallmark of Alzheimer's disease (AD), neurons died from the effect of the most harmful mutation of this neurodegenerative disease. They showed that presenilin (PS) could be behind the origin of the disease without the need for Aβ. They maintain that it is time to update theories and redirect efforts.

The risk of developing multiple sclerosis (MS) is nearly four times as high for women as it is for men. And that relative risk has increased sharply over time. In 1955, women were only slightly more likely than men to develop MS. A research team at the University of Toronto and the Oklahoma Medical Research Foundation (OMRF) has gained new insights into possible causes for this increasing disparity.

Researchers have identified a gene associated with whether patients hospitalized with respiratory viral infections recover rapidly or face life-threatening complications. The gene has the potential to be used as a diagnostic tool or biomarker, which could help triage patients suffering from severe respiratory infections. Having such a biomarker would help clinicians in their early risk assessments to manage their intervention strategies.

“There are hundreds of strains of bird flu, and most of them don’t infect humans, or even mammals,” Stephen Cusack told BioWorld. “There are two main reasons for that.” To be able to cause an infection, a virus “has to be able to get into the cell, and for that it needs a receptor,” Cusack said. For influenza viruses, those receptors are hemagglutinin receptors, and they differ in subtle but important ways between birds and mammals.

Researchers in Japan were able to transfer genes from jellyfish into common fruit flies and discovered that the transferred gene suppressed an age-related intestinal issue in the flies. The findings suggest that studying genes specific to animals with high regenerative capability like jellyfish may uncover new mechanisms for rejuvenating stem cell function and extending the healthy lifespan of unrelated organisms.

Infection or cure? Scientists from Tel Aviv University and the University of Glasgow genetically modified the Toxoplasma gondii to bring a protein inside neurons. The novelty of using a protozoan that can travel from the gut to parasitize the CNS contrasts with the possibility of causing a disease. The scientists are already working on how to avoid it.

A strategy inspired by deficient HIV replication could be used as a treatment to reduce viral load in patients living with HIV and help control the pandemic of the retrovirus. Scientists from the University of California San Francisco want to use HIV against itself by using a parasitic version of the pathogen.