An experimental drug restored aging liver cells in rats, cutting levels of an Alzheimer's-linked protein in half and bringing bad cholesterol down to youthful levels, according to researchers at the University of Southern California. The findings suggest that rejuvenating the liver could help protect against both Alzheimer's disease and heart disease, a link that scientists had not expected.
The treatment also revived a previously unknown communication system that helps liver cells remove harmful substances from the bloodstream. The researchers described the discovery as surprising, since the work focused on the liver rather than the brain or the heart. The results come from studies in rats, and the source material does not indicate whether the same effects have been confirmed in humans.
The liver's role in clearing the blood is one reason the findings matter for disease prevention. Cholesterol that accumulates in the bloodstream is a known risk factor for heart disease, and a liver that works less efficiently with age may contribute to that buildup. By bringing bad cholesterol back to levels seen in younger animals, the drug points to a possible route for reducing that risk, though the research so far addresses the mechanism rather than clinical outcomes.
The Alzheimer's connection is equally significant. The protein whose levels were cut in half is linked to the disease, which is marked by the progressive loss of brain function. Reducing that protein in aging animals suggests that the liver may influence processes that reach beyond the organ itself, a possibility the researchers have highlighted as worth further study.
Separate research on Alzheimer's has pursued a different approach. A study published in Cell Biomaterials, led by Peisheng Xu at the University of South Carolina, describes a strategy that aims to replace lost neurons rather than only slow their decline. Current therapies can slow neuronal degradation but cannot replenish the loss of neuronal circuits in the brain. The team used a polymer nanogel platform called Nano-ERASER to deliver an antibody across the blood–brain barrier into astrocytes, a type of support cell, where it reduces a protein called PTBP1 and prompts those cells to become new neurons.
In laboratory tests, astrocytes grown in a dish were stripped of PTBP1 and converted into neurons, and the treatment also converted astrocytes in human brain organoids, lab-grown tissues that mimic a real brain. In mice engineered to develop Alzheimer's-like pathology, two injections of the treatment, called TN-PTBP1, were enough to reverse the disease trajectory, according to the study. The converted cells fired electrically in the way neurons do. The Xu team's work is a separate line of research from the USC liver study, and the two should not be read as the same experiment.