As they matured from prenatal to adult, heart cells reduced the number of nuclear pores by more than 60%. That decrease protected them from the consequences of stress, but also impaired their ability to regenerate. “These findings are an important advance in fundamental understanding of how the heart develops with age and how it has evolved to cope with stress,” senior author Bernhard Kühn, professor of pediatrics and director of the Pediatric Institute for Heart Regeneration and Therapeutics at the University of Pittsburgh School of Medicine, said in a press release. Kühn and his colleagues published those findings in the Oct. 24, 2022, issue of Developmental Cell.
There is little doubt that progress in many brain diseases is being hampered because many, maybe most, diagnostic categories do not reflect underlying brain processes. In other disease areas, modern genetic and genomic methods have arrived in the form of approved drugs, from KRAS inhibitors in cancer to PCSK9 inhibitors to lower cholesterol. But brain diseases are different. Psychiatry is simultaneously the most personal area of medicine, and the least precise.
Disrupted meiosis, the cell division process that leads to the production of reproductive cells in sexually reproducing organisms, led to a decline in overall health by triggering an accelerating aging signature in the roundworm Caenorhabditis elegans.
The work is “the first direct evidence that manipulating the health of reproductive cells leads to premature aging and a decline in healthspan,” senior author Arjumand Ghazi, an associate professor of pediatrics, developmental biology, and cell biology and physiology at the University of Pittsburgh and the University of Pittsburgh Medical Center (UPMC) Children’s Hospital, said in a press release.
At first blush, to say that depression occurs with other diseases may seem like belaboring the obvious. After all, to put it in the bluntest possible terms, it’s sad to be sick. But by looking more closely, it soon becomes clear that the association is stronger than that. The strongest association between depression and other diseases, Stefan Gold told the audience at the European College of Neuropsychopharmacology (ECNP) annual conference in Vienna this week, is “not necessarily the most severe or most immediately life-threatening disorders… [it’s] across the spectrum."
Psychiatric animal models are a challenge by their nature. Whether a drug is blocking tumor growth in a rodent is easy enough to measure, although still hard to translate. But how does one figure out what a mouse is thinking? Actually, one doesn’t. There is “no way in heck I’m going to claim that I can model a thought disorder in rodents, so forget about that,” Bita Moghaddam told her audience at the opening keynote of the European College of Neuropsychopharmacology (ECNP) annual conference this weekend. But other aspects of mental disorders, she argued, can be usefully modeled.
“Epilepsy is really a classical neurological disorder,” Lars Pinborg told the audience at the European College of Neuropsychopharmacology (ECNP) annual conference on Sunday. “Or is it?” Pinborg, of Rigshospitalet's The Neuroscience Center in Denmark, was chairing a session dedicated to an alternative hypothesis, summed up in the session title: “Is epilepsy a psychiatric disorder?”
Scientists from the Global Biobank Meta-Analysis Initiative (GBMI) , founded in 2019, have published initial results in the Oct. 12, 2022 issue of Cell Genomics. In a series of papers, the investigators showed that the data collected by multiple biobanks could be harmonized and jointly analyzed, despite initial differences in recruitment strategies, sample collection, and definitions of diseases. Joint analysis identified new risk loci for more than a dozen common diseases, while another paper showed that such joint analysis could also be used to identify such loci for the rare disease idiopathic pulmonary fibrosis (IPF).
Researchers at the University of Cincinnati have published data showing that in patients with dominantly inherited Alzheimer’s disease-causing mutations, high levels of soluble amyloid-β42 (Aβ42) in the cerebrospinal fluid predicted a reduced risk of developing dementia over three years.
Researchers at the University of Cincinnati have published data showing that in patients with dominantly inherited Alzheimer’s disease (AD)-causing mutations, high levels of soluble amyloid-β42 (Aβ42) in the cerebrospinal fluid (CSF) predicted a reduced risk of developing dementia over 3 years. Their work, which appeared in the Oct. 4, 2022, print issue of the Journal of Alzheimer’s Disease after earlier publication online, suggests that the problem with amyloid in AD may be a lack of soluble amyloid-β, rather than a surfeit of plaques.
By independently manipulating the lifespan of worms and one of its purported biomarkers, namely, the cessation of vigorous movement (CVM), investigators at the Center for Genomic Regulation (CRG) in Barcelona have demonstrated that the two are driven by partly independent processes.
