In 2022, neuroscience research made significant advances by understanding the role of large-scale neuronal connections in disorders. So did cancer research.
The first in vivo cell atlas of senescent tissue in skeletal muscle has identified the damaging properties of these cells and explained why they block muscle regeneration. According to a study at Pompeu Fabra University led by scientists from Altos Labs Inc., cell damage caused the senescence of the cells, which secreted toxic substances into the surrounding microenvironment, causing fibrosis and preventing tissue regeneration.
Alzheimer’s disease has a higher incidence in women. This sex difference was associated with a modification of certain proteins of the immune system. According to a recent study, the drop in estrogen with menopause increased the expression in the brain of a neurotransmitter, nitric oxide (NO), generating the S-nitrosylation of complement factor C3 (abbreviated SNO-C3), which activated the microglia.
Liver damage arrests growth mediated by the somatotroph axis, which prevents liver cell death and inflammation, but increases fibrosis in nonalcoholic fatty liver disease (NAFLD). The explanation for this effect could lie in the relationship between the activating transcription factor 3 (ATF-3) and insulin-like growth factor 1 (IGF-1), according to a study from the University of California at Berkeley.
A combination of bioengineering techniques on normal cell binding proteins could be the method of the future for selective cell binding. Scientists at the University of California, San Francisco (UCSF) have created a synthetic glue based on the expression of membrane receptors to establish the desired connection between cells. The results may be applied in different fields of cell biology or biomedicine, such as regeneration and wound repair, including the nervous system, or cancer.
When a drug prevents bacteria from synthesizing their own folate, an essential compound for their survival, they take it directly from the host. This antibiotic resistance mechanism had not been detected until now because bacteria behave differently in the laboratory than they do in vivo during an infection.
When a drug prevents bacteria from synthesizing their own folate, an essential compound for their survival, they take it directly from the host. This antibiotic resistance mechanism had not been detected until now because bacteria behave differently in the laboratory than they do in vivo during an infection.
Scientists from the Icahn School of Medicine at Mount Sinai have found a sexual dimorphism of depression based on the different expression of a molecule that could be developed as a therapeutic strategy. “There is a big sex difference in depression. Women are much more likely to have depression than men. They tend to have different subsets of symptoms. They tend to respond better to different antidepressants, and the depression tends to be more severe,” Orna Issler, the first author of the study and a postdoctoral researcher at the Nash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, told BioWorld. Their project, directed by Eric Nestler, a professor of neuroscience and director of the Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai, had the aim to understand the biology of these sex differences of depression and to find therapeutic targets for it.
Retrotransposons could have a main role in the development of drug resistance in response to cancer treatment, according to a new study out of the Roswell Park Comprehensive Cancer Center. The transposition of DNA elements triggers an inflammatory response involved in the survival of cancer cells, a mechanism that could be blocked applying reverse transcriptase inhibitors, a class of drugs better known as anti-HIV medications.
Does cancer cause autoimmune disease or is it the other way around? In looking at the question of which comes first, the chicken or the egg, researchers at the Garvan Institute of Medical Research in Australia found that a genetic mutation that alters immune cells in leukemia is behind certain autoimmune disorders.
