Sometimes there are slightly different versions, or sequences of genes. There are several versions of the apolipoprotein E (APOE) gene, for example. One of them, called APOE4, has been linked to a much higher risk of developing Alzheimer’s disease, and carriers often have worse forms of the disease compared to carriers of other forms like APOE3. There are immune cells in the brain called microglia that help protect the brain from damage and harm. But when APOE4 is expressed, microglia seem to start to cause inflammation, and misfolded proteins to form in the brain, which can lead to serious problems. The findings have been reported in Cell Stem Cell.

In this work, the researchers developed a mouse model that could generate the human APOE4 protein in their brains. Next, the investigators eliminated microglia from these mouse brains. The formation of two misfolded proteins that are hallmarks of Alzheimer’s diseases: amyloid and tau, was halted.

Can therapy rewire the brain? For individuals struggling with both depression and obesity, a new Stanford Medicine study says yes—when the therapy is the right fit. Researchers found that cognitive behavioral therapy focused on problem-solving reduced depression symptoms in a third of participants and altered their brain activity in ways that could predict longer-term benefits. The findings have been published in Science Translational Medicine.

Depression affects millions of people worldwide and becomes particularly challenging to treat when paired with obesity, a condition that complicates recovery and worsens outcomes. Previous research has suggested that brain regions associated with cognitive control—areas responsible for regulating emotions and behaviors—might influence how individuals respond to therapy.

This study aimed to determine whether a therapy specifically designed to engage these brain circuits could lead to sustained improvements in depression symptoms, particularly in individuals with comorbid depression and obesity. The researchers also investigated whether early changes in brain activity could predict long-term therapeutic success, paving the way for more personalized treatment strategies.

It’s been more than three decades, but still there are only two treatments for a stroke: either rapid use of a clot-busting medication called tPA or surgical removal of a clot from the brain with mechanical thrombectomy. However, only 5% to 13% percent of stroke cases are actually eligible for these interventions.

“We need to be persistent with our research to find a new therapy for stroke,” says Rajkumar Verma, M.Pharm., Ph.D., assistant professor, Department of Neuroscience at UConn School of Medicine working in cross-campus collaboration with Professor Raman Bahal Ph.D. of the Department of Pharmaceutical Sciences in the UConn School of Pharmacy. “Stroke research is hard and challenging to do. But without trying we won’t make progress. We need to keep trying. UConn is determined to keep trying.”

In addition to being life-threatening, stroke is the major cause of long-term disability worldwide.

Scientists have discovered your cholesterol levels could be significantly linked to your risk of developing dementia. And it’s not just high cholesterol that matters: fluctuating levels over several years could increase your chances of the disease by 60 per cent, suggests a new study of 10,000 people.

The research also suggests that, even if you don’t develop dementia, a large cholesterol variability – swinging from high to low levels – is linked to an increased risk of general cognitive decline by 23 per cent.