A newly studied hormone is revealing an unexpected connection between metabolism and the brain.

How does Alzheimer’s target specific brain cells? Researchers are building a multiscale model of the hippocampus to map neuronal loss and cognitive decline.

New research has linked levels of vitamin D in midlife with toxic tangles of tau protein that accumulate in the brains of those with Alzheimer’s disease.

A statistical analysis of blood samples and brain scans from 793 adults showed that the more vitamin D in someone’s system in middle age, the lower the amount of tau protein tangles they tended to have years later.

The finding comes from an international team of researchers, and while it doesn’t prove direct cause and effect, it suggests an association that’s worth looking at.

A new Yale School of Medicine (YSM) study has uncovered surprising new details about how our eyes process what we see. When we look at something, our visual system breaks down different aspects of the scene—such as color, contrast, and motion—and processes those components separately. It’s called parallel visual processing and it’s what allows our brains to work out what we’re seeing so quickly.

This separation of information starts in the retina, and scientists have thought that separation is maintained as the information travels through the visual system. But in a study published in Neuron, researchers have found that information channels are more integrated than previously thought. This may help cells process weak visual signals, such as low-light conditions, the researchers say.

“We found that while different channels can deliver their own features, they’re also interconnected by underlying electrical circuitry,” says Yao Xue, Ph.D., a postdoctoral fellow in the department of ophthalmology and visual science at YSM and the study’s first author.

During intensive cancer treatment, children, adolescents and young adults are exposed to numerous toxicities and psychosocial stressors that can cause psychosocial distress and impair mental health. The maintenance or rapid recovery of mental health during and after exposure to significant stressors has been defined as resilience. To date, resilience research has focused primarily on cross-sectional assessment of specific, trait-like resilience factors and concepts in long-term survivors of childhood cancer, typically omitting the influence of context-specific biopsychosocial stressors and resilience dynamics throughout treatment. Little is known about outcome-based resilience and mental health resources in childhood cancer patients undergoing cancer treatment. In addition, specific instruments for age-appropriate assessment of resilience in childhood cancer patients are lacking. To address this gap, within the EU Horizon 2020-funded FORTEe project, we developed a novel self-report instrument for longitudinal assessment of resilience in children, adolescents, and young adults with cancer, featuring age-appropriate items tailored to their specific contexts.

An interdisciplinary team of psychologists, psychiatrists and pediatric oncologists developed an age-appropriate self-report instrument to assess resilience longitudinally in children, adolescents, and young adults undergoing cancer treatment. Following current resilience research frameworks, resilience is defined as the ratio of changes in mental health problems to stressor exposure. Accordingly, the measure comprises two domains: mental health problems (anxiety, depression, distress, fatigue) and stressor exposure (daily hassles, cancer-related stressors), with stressors rated for both frequency and intensity.

The Mainz Resilience Assessment in Childhood Cancer (MRAcc) consists of three age-specific versions (children 5–11 years, adolescents 12–17 years, young adults 18–21 years), each including the sections: ‘Emotions & Distress’, ‘Fatigue’, and ‘Situations & Experienced Stress’. It is available in German and English and uses either five-point-Likert scales or visual analogue scales presented as thermometers.

Carrying one or two copies of the APOE4 gene variant significantly increases the risk of developing Alzheimer’s, and a new study reveals how APOE4 can change neuron activity – potentially many years before symptoms such as memory loss start showing.

In young mice bred to have the APOE4 gene, researchers found specific neurons were smaller and more hyperactive in parts of the brain’s memory center, the hippocampus.

What’s more, they were able to identify a protein, Nell2, contributing to the disruption – and a potential pathway to reverse the damage in advanced cases.