Dementia is a brain disease that affects around 55 million people worldwide and is characterized by the loss of cognitive functions like memory and reasoning.

The classic, early cognitive symptoms of dementia – like misplacing valuable objects, forgetting names, and finding planning difficult – can creep up slowly over time.

But there are other, more noticeable changes to the body that correlate with dementia risk and can be picked up over a decade before diagnosis. Recent research has found that hearing difficulties may be a warning sign of dementia that arises years before other symptoms of the disease.

A deep slumber might help buffer against memory loss for older adults facing a heightened burden of Alzheimer’s disease, new research from the University of California, Berkeley, suggests.

Deep sleep, also known as non-REM slow-wave sleep, can act as a “cognitive reserve factor” that may increase resilience against a protein in the brain called beta-amyloid that is linked to memory loss caused by dementia. Disrupted sleep has previously been associated with faster accumulation of beta-amyloid protein in the brain. However, the new research from a team at UC Berkeley reveals that superior amounts of deep, slow-wave sleep can act as a protective factor against memory decline in those with existing high amounts of Alzheimer’s disease pathology —a potentially significant advance that experts say could help alleviate some of dementia’s most devastating outcomes.

“With a certain level of brain pathology, you’re not destined for cognitive symptoms or memory issues,” said Zsófia Zavecz, a postdoctoral researcher at UC Berkeley’s Center for Human Sleep Science. “People should be aware that, despite having a certain level of pathology, there are certain lifestyle factors that will help moderate and decrease the effects.

Sound waves can cross the blood-brain barrier and could deliver chemotherapy to complex and treatment-resistant glioblastomas.

High-grade gliomas functionally remodel neural circuits in the human brain, promoting tumour progression and impairing cognition.

CHICAGO, May 3 (Reuters) — An experimental Alzheimer’s drug developed by Eli Lilly and Co (LLY.N) slowed cognitive decline by 35% in a late-stage trial, the company said on Wednesday, providing what experts say is the strongest evidence yet that removing sticky amyloid plaques from the brain benefits patients with the fatal disease.

Lilly’s drug, donanemab, met all goals of the trial, the company said. It slowed progression of Alzheimer’s by 35% compared to a placebo in 1,182 people with early-stage disease whose brains had deposits of two key Alzheimer’s proteins, beta amyloid as well as intermediate levels of tau, a protein linked with disease progression and brain cell death.

The study also evaluated the drug in 552 patients with high levels of tau and found that when both groups were combined, donanemab slowed progression by 29% based on a commonly used scale of dementia progression known as the Clinical Dementia Rating Scale (CDR-SB).

Our research found that concussion was associated with increased functional connectivity between the thalamus and the rest of the brain very shortly after injury, when compared to 76 healthy control subjects.

In other words, the thalamus was trying to communicate more as a result of the injury. This was despite routine MRI and CT imaging showing no structural changes in the brain.

While many of us would assume that more connectivity in the brain is a good thing, research looking at more severe head injuries indicates that greater connectivity between brain regions might actually be a sign of the brain trying to compensate and offset damage across the brain.