Researchers have linked a specific type of body fat to the abnormal proteins in the brain that are hallmarks of Alzheimer’s disease up to 20 years before the earliest symptoms of dementia appear, according to a study being presented at the annual meeting of the Radiological Society of North America (RSNA).

The researchers emphasize that lifestyle modifications targeted at reducing this fat could influence the development of Alzheimer’s disease.

“This crucial result was discovered because we investigated Alzheimer’s disease pathology as early as midlife—in the 40s and 50s—when the disease pathology is at its earliest stages, and potential modifications like weight loss and reducing visceral fat are more effective as a means of preventing or delaying the onset of the disease,” said lead study author Mahsa Dolatshahi, M.D., M.P.H., post-doctoral research associate at Mallinckrodt Institute of Radiology (MIR) at Washington University School of Medicine in St. Louis, Missouri.

Vanderbilt University Medical Center-led research reveals subtle changes in the visual pathways of individuals with chronic mild traumatic brain injury (TBI), even when standard eye examinations show no abnormalities. These findings include structural and functional deficits despite participants showing normal visual acuity during clinical examination.

Mild TBI accounts for approximately 3 million cases in the U.S. each year. Up to 85% of TBI patients, regardless of injury severity, report visual disturbances such as light sensitivity, blurred vision, or difficulty reading. Persistent symptoms including memory problems, irritability, or slowed thinking often impact quality of life. Despite these symptoms, many individuals display no abnormalities during routine clinical evaluations such as fundus examinations.

In a case-control study, “Primary Visual Pathway Changes in Individuals With Chronic Mild Traumatic Brain Injury,” published in JAMA Ophthalmology, researchers reported that 78% of participants with mild TBI exhibited visual deficits when evaluated with a comprehensive battery of tests.

Long thought to be sterile, our brains are now believed to harbour all sorts of micro-organisms, from bacteria to fungi. How big a part do they play in Alzheimer’s and similar diseases?

Although it is widely recognized that sleep boosts cognitive performance, the neural mechanisms underlying this effect—especially those associated with non-rapid eye movement (NREM) sleep—are still not well understood.

A new study by a team of researchers at Rice University and Houston Methodist’s Center for Neural Systems Restoration and Weill Cornell Medical College, coordinated by Rice’s Valentin Dragoi, has nonetheless uncovered a key mechanism by which sleep enhances neuronal and behavioral performance, potentially changing our fundamental understanding of how sleep boosts brainpower.

The research, published in Science, reveals how NREM sleep — the lighter sleep one experiences when taking a nap, for example — fosters brain synchronization and enhances information encoding, shedding new light on this sleep stage. The researchers replicated these effects through invasive stimulation, suggesting promising possibilities for future neuromodulation therapies in humans. The implications of this discovery potentially pave the way for innovative treatments for sleep disorders and even methods to enhance cognitive and behavioral performance.