Nature neuroscience · 2025
Protective exercise responses in the dentate gyrus of Alzheimer's disease mouse model revealed with single-nucleus RNA-sequencing.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
da Rocha Joana F, Lance Michelle L, Luo Renhao, Schlachter Pius, Moreira Luis, Iqbal Mohamed Ariff, Kuhn Paula, Gardner Robert S, Valaris Sophia, Islam Mohammad R, Gassner Gabriele M, Mazuera Sofia, Healy Kaela, Shastri Sanjana, Hibbert Nathaniel B, Moran-Figueroa Kristen V, Haley Erin B, Pfeiffer Ryan D, Aygar Sema, Kastanenka Ksenia V, Brase Logan, Harari Oscar, Benitez Bruno A, Tucker Nathan R, Wrann Christiane D
Аннотация
Exercise's protective effects in Alzheimer's disease (AD) are well recognized, but cell-specific contributions to this phenomenon remain unclear. Here we used single-nucleus RNA sequencing (snRNA-seq) to dissect the response to exercise (free-wheel running) in the neurogenic stem-cell niche of the hippocampal dentate gyrus in male APP/PS1 transgenic AD model mice. Transcriptomic responses to exercise were distinct between wild-type and AD mice, and most prominent in immature neurons. Exercise restored the transcriptional profiles of a proportion of AD-dysregulated genes in a cell type-specific manner. We identified a neurovascular-associated astrocyte subpopulation, the abundance of which was reduced in AD, whereas its gene expression signature was induced with exercise. Exercise also enhanced the gene expression profile of disease-associated microglia. Oligodendrocyte progenitor cells were the cell type with the highest proportion of dysregulated genes recovered by exercise. Last, we validated our key findings in a human AD snRNA-seq dataset. Together, these data present a comprehensive resource for understanding the molecular mediators of neuroprotection by exercise in AD.