How the nervous system activates repair after spinal cord injury
Peer-Reviewed Publication
Updates every hour. Last Updated: 2-Jun-2026 04:16 ET (2-Jun-2026 08:16 GMT/UTC)
After a spinal cord injury, cells in the brain and spinal cord change to cope with stress and repair tissue. A new study from Karolinska Institutet, published in Nature Neuroscience, shows that this response is controlled by specific DNA sequences. This knowledge could help develop more targeted treatments.
LMU-Scientists uncover key proteins that control how Toxoplasma gondii assembles the machinery it uses to invade host cells.
Results from a VHIO-led study show that MYC targeting by Omomyc induces tumor DNA damage in patient-derived preclinical models of BRCA1/2-mutated triple-negative breast cancer.
Omomyc-induced DNA damage, combined with PARP inhibitors (PARPi) that block single-stranded DNA repair mechanisms, creates a synergistic effect against cancer cells that could help to overcome PARPi resistance in this patient population.
A new Genomic Press Interview with Prof. Dr. Paul Lucassen shares insights from his research spanning 30 years in which he explores how the adult brain continues to produce new neurons, and how this process, and other plasticity-related aspects like cognition, are modulated by (early life) stress, exercise, nutrition, and inflammation, revealing unexpected connections between early childhood experiences and later vulnerability to psychiatric disorders and dementia. His work offers hope that brain plasticity can maybe one day be harnessed for therapeutic and preventive approaches.
A Curtin University-led study has found that where Australians live has a measurable influence on their body weight, with local food environments and neighbourhood design playing a big part in shaping health outcomes.
A sweeping review article published in Genomic Psychiatry examines whether current strategies for studying aging actually capture what scientists claim to measure. Dr. Dan Ehninger and Dr. Maryam Keshavarz from the German Center for Neurodegenerative Diseases (DZNE) in Bonn, Germany, analyze cross-species mortality data spanning humans, nonhuman primates, rodents, dogs, fish, fruit flies, and nematode worms to demonstrate that lifespan extension frequently reflects delayed onset of specific diseases rather than genuine slowing of biological aging. Their systematic evaluation of studies supporting the influential hallmarks of aging framework reveals that between 56 and 99 percent of phenotypes cited as evidence were examined only in aged animals, lacking the experimental designs needed to distinguish true aging effects from age-independent baseline shifts. The authors propose refined methodological approaches that could transform how researchers identify and validate interventions targeting the aging process itself.