Imagine your brain as a bustling city, and Alzheimer’s disease as a disruptive force wreaking havoc on its streets. But fear not! Scientists have found a way to restore order and functionality using an exciting therapy called transcranial direct current stimulation (tDCS). In a recent study, researchers applied tDCS to the prefrontal cortex of mice with Alzheimer’s disease, and the results were astonishing. Not only did the tDCS treatment improve spatial learning and memory in the mice, but it also led to changes in their brainwave patterns. The mice exhibited decreased slow-wave activity (delta waves) and increased fast-wave activity (gamma waves) during memory retrieval tasks. These changes suggest that tDCS can effectively accelerate brain activity and enhance cognitive function in individuals with Alzheimer’s disease. These findings hold great promise for developing new treatments for this devastating condition. If you’re intrigued by the power of stimulating brain cells, dive into the full research article to uncover more about this groundbreaking study!

Alzheimer’s disease (AD) is a leading cause of dementia in the elderly, with no effective treatment currently available. Transcranial direct current stimulation (tDCS), a non-drug and non-invasive therapy, has been testified efficient in cognitive enhancement. This study aims to examine the effects of tDCS on brain function in a mouse model of AD. The amyloid precursor protein (APP) and presenilin 1 (PS1) transgenic mice (7–8 months old) were subjected to 20-min anodal and cathodal tDCS (atDCS and ctDCS; 300 μA, 3.12 mA/cm2) for continuous five days. tDCS was applied on the left frontal skull of the animals, targeting on their prefrontal cortex (PFC). Behavioral performances were assessed by open-field, Y-maze, Barnes maze and T-maze paradigms; and their PFC electroencephalogram (EEG) activities were recorded under spontaneous state and during Y-maze performance. Behaviorally, atDCS and ctDCS improved spatial learning and/or memory in AD mice without affecting their general locomotion and anxiety-like behaviors, but the effects depended on the testing paradigms. Interestingly, the memory improvements were accompanied by decreased PFC EEG delta (2–4 Hz) and increased EEG gamma (20–100 Hz) activities when the animals needed memory retrieval during task performance. The decreased EEG delta activities could also be observed in animals under spontaneous state. Specifically, atDCS increased PFC EEG activity in the alpha band (8–12 Hz) for spontaneous state, whereas ctDCS increased that in alpha-beta band (8–20 Hz) for task-related state. In addition, some EEG changes after ctDCS could be found in other cortical regions except PFC. These data indicate that tDCS can reverse the situation of slower brain activity in AD mice, which may further lead to cognitive improvement. Our work highlights the potential clinical use of tDCS to restore neural network activity and improve cognition in AD.

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