This cohort study of breast cancer survivors found a lower risk of Alzheimer dementia (AD) compared with cancer-free controls, despite common concerns about cognitive decline after treatment. The findings suggest certain cancer treatments potentially have benefits for lower AD risk. Further research is needed to assess the long-term risk of AD in this population. 

A newly identified brain circuit has provided insights into how animals recover from lost sleep. According to a new study in mice, neurons in a specific region in the thalamus become active during sleep deprivation and help trigger restorative deep sleep to maintain sleep homeostasis. Sleep is a near-universal biological rhythm that most animals experience. When sleep is insufficient or delayed, a sleep “debt” accumulates, leading to deeper and longer sleep to restore sleep homeostasis. However, the neuronal mechanisms that trigger this recovery sleep remain poorly understood. “Many neurological and psychiatric disorders, such as Alzheimer’s disease, schizophrenia, and traumatic injury, are associated with sleep loss and/or inappropriate sleepiness,” write Nichole Gilette and Jonathan Lipton in a related Perspective. “There is, therefore, considerable translational potential in the identification of a potential source of the brain’s dedicated mechanisms for reestablishing sleep-wake balance.” In this study, Sang Soo Lee and colleagues identify a neural circuit in the brain’s thalamus that is crucial for the homeostatic regulation of sleep after sleep deprivation. Lee et al. mapped neural circuits connected to known sleep-promoting brain regions in mice and discovered a subset of excitatory neurons in the medial thalamic nucleus reuniens (mRE) that are activated during sleep deprivation. When these mRE neurons were experimentally activated using chemogenetic and optogenetic tools, mice exhibited deeper and more prolonged non-REM sleep several hours later, suggesting that these neurons don’t directly induce sleep but instead regulate sleep homeostasis. Activation of mRE neurons also enhanced nesting and grooming behaviors, which are typical pre-sleep activities in rodents. What’s more, when researchers recorded neuronal activity during extended wakefulness, they observed increased firing in the mRE, which subsided during subsequent recovery sleep. This pattern contrasts with conventional sleep-promoting neurons, which are typically most active during sleep itself, suggesting that the circuit is dedicated to reestablishing sleep homeostasis, rather than just regulating sleep-wake cycles.

Scientists at the USC Leonard Davis School of Gerontology have discovered a key connection between high levels of iron in the brain and increased cell damage in people who have both Down syndrome and Alzheimer’s disease. In the study, researchers found that the brains of people diagnosed with Down syndrome and Alzheimer’s disease (DSAD) had twice as much iron and more signs of oxidative damage in cell membranes compared to the brains of individuals with Alzheimer’s disease alone or those with neither diagnosis. The results point to a specific cellular death process that is mediated by iron, and the findings may help explain why Alzheimer’s symptoms often appear earlier and more severely in individuals with Down syndrome.