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Enriched environment improves memory function by promoting synaptic remodeling in vascular dementia rats.

Shuang Lin¹, Chuan-Jie Wang², Peng-Kun Yang¹

¹Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai, China.

Brain Research Bulletin

|February 20, 2025

Summary

Enriched environments (EE) significantly improve cognitive function and synaptic plasticity in a rat model of vascular dementia (VaD). This non-pharmacological approach restores memory by enhancing neurotrophic factors and synaptic structure.

Keywords:

BDNF Enriched environment FNDC5 Synapse Vascular dementia

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Area of Science:

Neuroscience
Cognitive Science
Pathology

Background:

Vascular dementia (VaD) is a major cause of cognitive decline, marked by memory loss and other deficits.
Cerebrovascular pathology underlies VaD, driving significant neurological impairment.
Enriched environments (EE) show potential for cognitive restoration via enhanced neuroplasticity.

Purpose of the Study:

To investigate the efficacy of enriched environments (EE) in ameliorating cognitive deficits in a rat model of vascular dementia (VaD).
To explore the underlying neuromorphological and molecular mechanisms of EE intervention in VaD.

Main Methods:

Vascular dementia was induced in rats via bilateral common carotid artery ligation (BCCAO).
Rats were assigned to sham-operated, VaD, or VaD with EE groups.
Behavioral tests (Morris water maze), transmission electron microscopy, and molecular analyses (PSD95, PGC-1α/FNDC5/BDNF pathway) were employed.

Main Results:

EE intervention significantly improved spatial learning and memory in the Morris water maze.
Neuromorphological analysis revealed increased synaptic density and PSD thickness in the hippocampus (CA1 region).
EE upregulated PSD95 expression and elevated levels of PGC-1α, FNDC5, and BDNF.

Conclusions:

Enriched environments offer a promising non-pharmacological strategy for treating vascular dementia.
EE promotes cognitive recovery by enhancing synaptic plasticity and activating key neurotrophic pathways.
Findings support further investigation of EE for clinical application in VaD patients.