Past psychology studies suggest that people tend to remember emotional events, such as their wedding, the birth of a child or traumatic experiences, more vividly than neutral events, such as a routine professional meeting. While this link between emotion and the recollection of past events is well-established, the neural mechanisms via which emotional states strengthen memories remain poorly understood.

Researchers at the University of Chicago and other institutes carried out a study aimed at better understanding these mechanisms. Their findings, published in Nature Human Behaviour, suggest that emotional states facilitate the encoding of memories by increasing communication between networks of brain regions.

“Emotional experiences tend to be ‘sticky,’ meaning that they endure in our memories and shape how we interpret the past, engage with the present, and anticipate the future,” Yuan Chang Leong, senior author of the paper, told Medical Xpress.

When we get sick, with the flu, say, or pneumonia, there can be a period where the major symptoms of our illness have resolved but we still just don’t feel great.

“While this is common, there’s no real way to quantify what’s going on,” says Nikolai Jaschke, MD, Ph.D., who recently completed a postdoctoral fellowship at Yale School of Medicine (YSM) in the lab of Andrew Wang, MD, Ph.D., associate professor of internal medicine (rheumatology). “And unfortunately, we lack therapeutic tools to support people in this state.”

Jaschke noticed this while taking care of patients recovering from acute illnesses and, when he joined Wang’s lab, he began studying what was happening in the body during recovery. Through this work, Jaschke, Wang, and their colleagues uncovered a gut-to-brain signaling pathway in mice that restricts appetite—specifically for protein—during recovery. They published their findings on Nov. 4 in Cell.

A new study examining real-world hospital data reveals early indicators of who is most likely to benefit from Cobenfy, the first new schizophrenia drug mechanism approved in 50 years.

Few moments are more heartbreaking for families of Alzheimer’s disease patients than when a loved one no longer recognizes them. New research from the University of Virginia School of Medicine published in Alzheimer’s & Dementia may reveal why that happens and offer hope for prevention.

UVA’s Harald Sontheimer, graduate student Lata Chaunsali and their colleagues found that when protective structures around brain cells break down, people may lose the ability to recognize loved ones. In lab studies, keeping these structures intact helped mice remember one another.

“Finding a structural change that explains a specific memory loss in Alzheimer’s is very exciting,” said Sontheimer, chair of UVA’s Department of Neuroscience and member of the UVA Brain Institute. “It is a completely new target, and we already have suitable drug candidates in hand.”

A collection of studies that chart how mammalian brain cells grow and differentiate is a ‘very valuable’ tool for neuroscientists.

Drugs that act on NMDA (N-methyl-D-aspartate) receptors, which are essential for learning, memory and moment-by-moment consciousness, are key for treating neuropsychiatric disorders. These drugs were developed based on the assumption that the proportion of calcium in the current produced by these receptors remains constant. That assumption turns out to be false, according to University at Buffalo research published last month in the Proceedings of the National Academy of Sciences.

“Our research reveals that small variations in the brain environment in which NMDA receptors operate can increase or decrease the amount of calcium in the currents fluxed by these receptors,” explains Gabriela K. Popescu, Ph.D., corresponding author and professor of biochemistry in the Jacobs School of Medicine and Biomedical Sciences at UB. “This, in turn, could mean the difference between normal and impaired learning, memory and cognition, symptoms that accompany many neuropsychiatric conditions.”