Uncertainty about a possible future threat disrupts our ability to avoid it or to mitigate its negative impact, and thus results in anxiety. Here, we focus the broad literature on the neurobiology of anxiety through the lens of uncertainty. We identify five processes essential for adaptive anticipatory responses to future threat uncertainty, and propose that alterations to the neural instantiation of these processes results in maladaptive responses to uncertainty in pathological anxiety. This framework has the potential to advance the classification, diagnosis, and treatment of clinical anxiety.
Scientists at Johns Hopkins Medicine say results of a new study are advancing efforts to exploit a new target for Alzheimer’s disease: a protein that manufactures an important gas in the brain.
Experiments conducted in genetically engineered mice reinforce that the protein, Cystathionine γ-lyase, or CSE—ordinarily known for producing hydrogen sulfide gas responsible for the foul smell of rotten eggs—is critical for memory formation, says Bindu Paul, M.S., Ph.D., associate professor of pharmacology, psychiatry and neuroscience at the Johns Hopkins University School of Medicine, who led the study.
The new research, published in Proceedings of the National Academy of Sciences, was designed to better understand the basic biology of the protein, and its value as a novel target for drugs that boost the expression of CSE in people to help keep brain cells healthy and slow neurodegenerative disease.
In this work, Vigo et al. demonstrate that norepinephrine (NE) promotes myeloid hematopoiesis in BM and regulates thymic Tregs via B3ARs in EAE. B3ARs are controlled by hypothalamic AgRP neurons, which are dysfunctional in EAE. Serum levels of AgRP are elevated in people with MS and correlate with disease severity.
Memories and learning processes are based on changes in the brain’s neuronal connections and, as a result, in signal transmission between neurons. For the first time, DZNE researchers have observed an associated phenomenon in living brains – specifically in mice. This mechanism concerns the cellular pulse generator for neuronal signals (the “axonal initial segment”) and had previously only been documented in cell cultures and in brain samples. A team led by neuroscientist Jan Gründemann reports on this in the journal Nature Neuroscience, alongside experts from Switzerland, Italy, and Austria. Their study sheds light on the brain’s ability to adapt. Next, the researchers intend to investigate the significance of these findings in Alzheimer’s disease.
In the brain, neurons branch out and connect with each other to form a network through which electrical signals are actively exchanged. This network structure is an essential component of the brain’s “hardware” and is therefore fundamental to its function, especially with regard to learning processes and memory formation. However, this complex architecture and signal transmission across this network are not fixed; they can change as a result of experiences and events. This flexibility, also known as neuroplasticity, is the basis for the brain’s ability to adapt.
As memories are formed, the brain changes in measurable ways: synaptic “pulse generators” grow and shrink, revealing surprising insights from brain research.
