Immortality and eternal youth have been the stuff of myths and legends from ancient times on. Now, in the 21st century, real studies of current medicine could be applied to repair tissues and organs damaged by age. During the 11th Aging Research & Drug Discovery (ARDD) Meeting held at the University of Copenhagen at the end of August, scientists explained the molecular keys of rejuvenation, as many artists imagined in the past.

Aging is part of the life cycle and, although the effects are not manifest until after adulthood, it actually occurs from birth. The concept of senescence has traditionally been associated with aging. However, an embryo has senescent cells. In that case, what is aging, how can it be measured, and from what point in the life cycle?

Aging is part of the life cycle and, although the effects are not manifest until after adulthood, it actually occurs from birth. The concept of senescence has traditionally been associated with aging. However, an embryo has senescent cells. In that case, what is aging, how can it be measured, and from what point in the life cycle?

Aging is part of the life cycle and, although the effects are not manifest until after adulthood, it actually occurs from birth. The concept of senescence has traditionally been associated with aging. However, an embryo has senescent cells. In that case, what is aging, how can it be measured, and from what point in the life cycle?

Since the publication of The Hallmarks of Aging in 2013, aging research has exploded. The field now has more than 300,000 articles on the biological signals of the effect of time on the body. What would Marty McFly, the legendary character from the Back to the Future saga who traveled with his DeLorean time machine from the ‘80s to the ‘50s, think if he visited 2024 and saw laboratories experimenting with techniques to turn back the biological clocks of cells or increase the lifespan of rejuvenated mice?

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.

Restoring glucose metabolism in astrocytes, which is impaired in Alzheimer’s disease (AD), has a direct effect on neurons, which replenish their fuel supply and resume synaptic activity. A group of scientists from Stanford University School of Medicine has revealed the pathway that explains where this efflux is interrupted and which molecules restore it in mouse models with amyloid and tau pathology. Their findings could help prevent the progression of this neurodegenerative disease.

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.

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.