Multisensory gamma stimulation enhances adult neurogenesis and improves cognitive function in male mice with Down Syndrome
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ABSTRACT:
PROVIDER: PRJNA1018259 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26083300_1.fastq.gz | Fastqsanger.gz | |||
| SRR26083300_2.fastq.gz | Fastqsanger.gz | |||
| SRR26083301_1.fastq.gz | Fastqsanger.gz | |||
| SRR26083301_2.fastq.gz | Fastqsanger.gz | |||
| SRR26083302_1.fastq.gz | Fastqsanger.gz |
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Project description:Multisensory Gamma Stimulation (MGS) has previously been linked with improved cognitive performance in mouse models and patients with Alzheimer´s Disease (AD). In this study, we aimed to investigate the effects of chronic exposure to MGS in Ts65Dn mice, a mouse model of Down Syndrome (DS). For three weeks, mice were exposed daily to one hour of multisensory audiovisual stimulation or, as a control, one hour of ambient light and sound. Mice receiving MGS showed improved object recognition and spatial working memory. To gain mechanistic insight into how MGS improves cognitive function in Ts65Dn mice, we conducted single-nuclei RNA-seq (snRNA-seq) of hippocampal samples from control and treated mice. We found upregulation of genes related to synaptic organization and downregulation of genes related to aging and AD. Moreover, we detected upregulation of neurogenesis-related genes in the dentate gyrus. We validated these observations by demonstrating increased adult neurogenesis following MGS treatment. A potential mechanism underlying this MGS-mediated increase in adult neurogenesis is increased mitochondrial fusion. Together, our data indicate that MGS can ameliorate cognitive impairment in DS mice through modulation of conserved gene regulatory signatures and enhanced neurogenesis in hippocampal regions. These findings suggest that multisensory 40 Hz stimulation may have potential as a therapeutic approach to boost cognitive performance in individuals with Down Syndrome.
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Project description:Gamma oscillations are disrupted in various neurological disorders, including Alzheimer's disease (AD). In AD mouse models, non-invasive audiovisual stimulation (AuViS) at 40 Hz enhances gamma oscillations, clears amyloid-beta, and improves cognition. We investigated mechanisms of circuit remodeling underlying these restorative effects by leveraging the sensitivity of hippocampal neurogenesis to activity in middle-aged wild-type mice. AuViS increased progenitor cell proliferation, neuronal differentiation and morphological maturation of newborn granule cells, promoting their synaptic integration. While visual or auditory stimuli alone induced dendritic growth, axonal changes required combined audiovisual stimulation. The actions of AuViS involved neurotrophin pathways, as shown by the lack of effect upon TrkB signaling blockade. These results reveal widespread plasticity mechanisms triggered by AuViS, a therapeutic approach currently proposed for treating neurological disorders in humans.
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