Low-Intensity Brain Stimulation Shows Promise for Alzheimer's Neuron Health

In a groundbreaking study published in the *Neurophotonics* journal on June 30, 2025, researchers from the University of Queensland and the Wicking Dementia Research and Education Center at the University of Tasmania have found that low-intensity repetitive transcranial magnetic stimulation (rTMS) can enhance synaptic plasticity in mice models of Alzheimer's disease (AD). This research highlights a potential new avenue for improving cognitive functions in individuals suffering from this debilitating neurodegenerative condition.

Alzheimer's disease, which affects millions of older adults worldwide, is characterized by synaptic dysfunction that leads to declines in memory and cognitive abilities. According to Dr. Barbora Fulopova, a professor at the University of Queensland and the study's corresponding author, the capacity of the brain to regulate synaptic connections—termed synaptic plasticity—deteriorates in patients with AD, exacerbating symptoms over time. Currently, there are limited therapeutic options available to manage the condition effectively.

Repetitive transcranial magnetic stimulation (rTMS) employs electromagnetic pulses to stimulate specific brain areas non-invasively. Previous studies have indicated its potential in enhancing synaptic plasticity in healthy neural systems; however, the precise mechanisms at play in AD remained unclear until now. The research team utilized two-photon microscopy to observe changes in axonal boutons, which are specialized structures where neurons communicate, in a genetically modified mouse model that replicates AD-like symptoms in humans.

The study involved monitoring two types of excitatory boutons: terminaux boutons (TBs), which connect neighboring neurons, and en passant boutons (EPBs), found along axons that connect distal regions. The researchers discovered that while the density of TBs and EPBs remained comparable between the AD mouse model and healthy counterparts, the turnover rate of these boutons was significantly lower in the AD model prior to rTMS treatment. The buildup of amyloid plaques—a hallmark of Alzheimer's—was identified as a likely cause for this decreased functionality.

Following a single session of low-intensity rTMS, the researchers observed a notable increase in the turnover of TBs, with a remarkable 213% rise in the AD model mice as compared to pre-stimulation levels. In healthy wild-type mice, the turnover also increased significantly by 88%. However, this heightened turnover returned to baseline levels by the eighth day post-stimulation, indicating a temporary restoration of synaptic plasticity.

Dr. Fulopova emphasized the importance of this research, stating, "This study is the first to provide evidence of pre-synaptic boutons responding to rTMS in both healthy and Alzheimer’s-affected nervous systems. Given the established link between synaptic dysfunction and cognitive decline in dementia, our findings underscore rTMS's potential as a valuable addition to current AD management strategies."

While these findings are promising, further research is necessary to fully understand the underlying mechanisms and to explore the long-term effects of rTMS on cognitive functions in humans with Alzheimer's disease. The implications of this study may pave the way for targeted rTMS treatments that could enhance the quality of life for patients suffering from Alzheimer's and potentially other neurodegenerative diseases. In conclusion, the investigation into rTMS as a therapeutic intervention could represent a pivotal shift in the management of Alzheimer's disease, offering hope to millions affected by this condition.