While a gradual loss in muscle strength is a natural part of aging, for many older adults it’s more than just feeling a little weaker. Sarcopenia — a condition affecting nearly half of adults over 80 — involves a sharp decline in muscle size and strength, increasing the risk of falls and fractures, impacting overall health, life expectancy and quality of life.

Now, researchers at the University of Missouri have identified a game-changing solution. Their recent study suggests that a small molecule drug that targets a specific serotonin receptor could become the first neurotherapeutic treatment for sarcopenia — offering hope for older adults struggling to stay strong.

A new Penn Nursing study published in the Annals of the American Thoracic Society challenges conventional thought regarding the benefits of continuity in nursing care within intensive care units (ICUs). The researchers found that increased nurse continuity was not associated with a reduction in in-hospital mortality – in some shifts, it was even linked to a modest but statistically significant increase in mortality.

The neurotransmitter glutamate is essential for regulating everything from mood to memory, but it can also encourage a toxic buildup of protein, which can contribute to Alzheimer’s and related diseases. In a USC Stem Cell-led study published in Neuron, scientists describe a new approach for counteracting these devastating and often fatal neurodegenerative effects. Researchers made their discovery by studying lab mice as well as human brain “organoids,” which are rudimentary brain-like structures grown in the lab. The scientists produced these organoids from stem cells derived from healthy people as well as from patients with neurodegenerative diseases related to tau toxicity. When exposed to glutamate, the organoids—particularly the ones derived from patients with neurodegenerative diseases—exhibited a toxic buildup of tau protein as well as neurodegeneration and nerve cell death. Mice with a mutation in tau, which causes a common form of dementia, displayed similar pathologies. Many potential drugs have been developed to mitigate the neurodegenerative effects of glutamate toxicity, but they’ve had mixed results in clinical trials. Taking a different approach, the scientists screened for genes that respond to glutamate and identified a gene called KCTD20. When the scientists suppressed the activity of this gene in the organoids and in the mice, glutamate did not produce the same ill effects in terms of either tau buildup or neurodegeneration. Through additional experiments, the team discovered that suppressing this gene activated cellular compartments called lysosomes, which enveloped the toxic tau proteins and expelled them from the organoids’ cells.