Deep brain stimulation is used to treat movement disorders, but studies suggest it also affects memory. Scientists have uncovered its mechanism of action and identified a molecular pathway that could pave the way for new treatments.
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Researchers at Baylor College of Medicine in the United States studied Rett syndrome, a neurological disorder linked to a deficiency in the MeCP2 gene, which disrupts the growth of new neurons in mice, reduces dendrite formation, and impairs synaptic function. The researchers discovered that stimulating a specific brain region improves learning and memory abilities.
Dr. Jianrong Tan says, "We discovered that the Rett syndrome model shows impaired communication between neurons in the hippocampus, as well as disruption of signal transmission between them and altered ability to strengthen connections, a process known as synaptic plasticity."
A previous study by the team had shown that daily stimulation of the fornix, the brain pathway connecting the hippocampus to other brain regions, over a two-week period restored learning and memory abilities to normal levels. The treatment also contributed to increased production of new neurons.
The researchers in the new study focused on determining whether newly formed neurons are necessary for these benefits. To investigate, they inhibited the production of new neurons and observed that memory improvement ceased. This suggests that these cells need time to mature before they can contribute to memory enhancement.
Dr. Tan says: "The stimulation helped restore the morphological structure of newly formed neurons lacking the MECP2 protein, improved communication between neurons, and contributed to restoring the balance between excitatory and inhibitory signals."
According to the researchers, one of the key molecular components in this process is the KCC2 protein, the levels of which decrease when the MeCP2 protein is lost. KCC2 regulates the functional switch of the neurotransmitter GABA from excitatory to inhibitory. In the absence of this protein, the maturation of newly formed neurons is delayed.
The results also showed that activating the KCC2 protein mimics the effect of stimulation and improves memory performance.
Dr. Tan emphasizes that these results have so far been achieved only in a mouse model, noting the need for further studies to determine whether similar methods can be safely applied to humans.
The results were published in the journal Proceedings of the National Academy of Sciences
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