A new study has identified a specific gene, ATPPIF1, that is reactivated through exercise and supports neuroplasticity in the brain, potentially slowing Alzheimer’s disease progression. Researchers used single-nuclei RNA sequencing to map how brain cells in the hippocampus respond to aerobic activity, uncovering molecular pathways that may be targeted with future drug therapies.
The study found that exercising increases ATPPIF1 expression, which helps create new neurons and promotes neuron survival, synaptic function, and memory-related brain plasticity. This breakthrough offers hope for patients who cannot stay active due to frailty or advanced symptoms.
According to the study’s senior author, Christiane Wrann, “We know that exercise does many good things to the brain and against Alzheimer’s disease. Instead of prescribing the exercise, we actually want to activate these molecular pathways using pharmacology to improve cognitive function in these patients.”
The researchers plan to use gene therapy in human subjects to turn their discoveries into treatments. While exercise can benefit cognitive diseases like Alzheimer’s, there is still no cure. The study suggests that exercising before the onset of dementia may slow down cognitive decline, but its effects become less significant once dementia sets in.
This work was supported by funds from the National Institutes of Health.
Source: https://neurosciencenews.com/genetics-exercise-neuropharmacology-29370