Dr. Damian Young, investigator at Texas Children’s Duncan Neurological Research Institute (Duncan NRI) and director of the Center for Drug Discovery at Baylor College of Medicine, along with collaborators has been awarded a $6.7 million grant from the National Institute on Aging (NIA), part of the National Institutes of Health (NIH), to develop new approaches to rapidly identify potential treatments for Alzheimer’s disease and related dementias with the goal of accelerating the discovery of new therapies.

For centuries, the inability to regrow lost body parts has been considered a defining limitation of humans and other mammals. While animals like salamanders can regenerate entire limbs, humans are left with scar tissue.

But new research from the Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) suggests that this limitation may not be permanent. Instead, the capacity for regeneration may still exist — hidden within the body’s normal healing process.

Researchers at Pennington Biomedical Research Center provide critical insight into how the brain and body work together to regulate food intake, energy use and metabolism – offering important new analysis into the biology of obesity and metabolic health.

The study, “FGF21 signals through hindbrain neurons to alter food intake and energy expenditure during dietary protein restriction,” published in the journal Cell Reports and led by Pennington Biomedical Associate Executive Director for Basic Science Dr. Christopher Morrison and colleagues, focuses on Fibroblast Growth Factor 21 (FGF21), a hormone produced by the liver that helps the body adapt to changes in diet and nutritional status.

The acquisition of totipotency is a fundamental process in early mammalian development, characterized by zygotic genome activation (ZGA) and the transient expression of 2-cell-stage (2C) specific genes and retrotransposons, such as MERVL. While the Double Homeobox (DUX) family proteins (mouse Dux and human DUX4) are recognized as master transcription factors for this transition, the underlying biophysical mechanisms by which they orchestrate global chromatin remodeling and coordinate distal gene activation have remained elusive.

Temporomandibular joint (TMJ) osteoarthritis affects millions of people, yet the earliest molecular events behind the disease remain poorly understood. Researchers have now mapped how mechanical stress and disk displacement trigger cellular changes in the jaw joint’s synovium using advanced transcriptomic technologies. Their findings reveal inflammatory and fibrotic responses that may drive disease onset. The work provides a high-resolution cellular atlas of TMJ tissues, offering insights that could guide future therapies aimed at preventing joint degeneration.

Impaired wound healing and pathological scarring remain major clinical challenges, closely linked to dysregulation of the immune microenvironment.

Impaired wound healing and pathological scarring remain major clinical challenges, closely linked to dysregulation of the immune microenvironment. Aberrant macrophage polarization, persistent neutrophil activation, and dysfunctional T cell regulation have been demonstrated to critically shape wound resolution and fibrotic outcomes. However, conventional in-vitro models fail to recapitulate human-relevant immune responses, thereby limiting mechanistic insights into wound healing pathology and hindering therapeutic translation.

Human tumor organoids have advanced cancer modeling by preserving patient-specific heterogeneity and functional drug responses. However, translating organoid findings into routine decision-making remains challenging due to variability in culture conditions and incomplete reconstruction of the tumor microenvironment. In this review, we present a clear and actionable framework that positions tumor organoids as dynamic living biosensors, linking mechanistic studies, tumor microenvironment reconstruction, functional drug-response phenotyping, and precision-therapy decision-making.