Lycium barbarum Extract Enhanced Neuroplasticity and Functional Recovery in 5xFAD Mice via Modulating Microglial Status of the Central Nervous System

CNS Neuroscience & Therapeutics, 2024 · DOI: https://doi.org/10.1111/cns.70123 · Published: October 30, 2024

Simple Explanation

This study investigates the potential of Lycium barbarum extract (LBE), derived from goji berries, as a treatment for Alzheimer's disease (AD). The research focuses on how LBE affects the central nervous system (CNS) in mice genetically engineered to mimic AD. The study found that LBE treatment slowed the decline in cognitive, motor, and visual functions in the AD mice. It also observed changes in microglia, a type of immune cell in the brain, suggesting a shift towards a neuroprotective state. These findings suggest that LBE could be a beneficial anti-aging strategy for AD. It might work by enhancing neuroplasticity, reducing inflammation, and improving the clearance of amyloid-beta deposits in the brain.

Study Duration

2 months

Participants

5xFAD transgenic mice and wild-type littermates

Evidence Level

Not specified

Key Findings

1
LBE treatment significantly slowed the decline in cognitive, motor, and visual functions in 5xFAD mice.
2
Microglia in the brain, spinal cord, and retina of LBE-treated mice exhibited a neuroprotective state, with reduced Aβ deposition and decreased inflammatory cytokine levels.
3
LBE promoted Aβ uptake and degradation in primary microglia and the IMG cell line, while also elevating neuroprotective signals like p-Akt, p-Erk1/2, and p-CREB.

Research Summary

This study investigated the effects of Lycium barbarum extract (LBE) on the central nervous system (CNS) in 5xFAD transgenic mice, a model for Alzheimer's disease (AD). The objective was to assess LBE's potential to enhance neuroplasticity and functional recovery. The results indicated that LBE treatment slowed cognitive, motor, and visual function decline in the mice. This was associated with a shift in microglia to a neuroprotective state, reduced amyloid-beta (Aβ) deposition, and decreased inflammation in the brain, spinal cord, and retina. The study suggests that LBE can enhance neuroplasticity, reduce inflammation, and improve Aβ clearance by inducing a neuroprotective microglial phenotype throughout the CNS. This supports LBE's potential as an anti-aging strategy for AD.

Practical Implications

Potential Therapeutic Agent for AD

LBE may serve as a supplementary drug for AD treatment due to its multiple beneficial effects.

Neuroprotective Effects

LBE's ability to promote neuroprotective microglia may offer new insights into treating neurodegenerative diseases.

Anti-inflammatory Properties

The extract's capacity to reduce inflammation and modulate immune responses could be valuable in managing neurodegenerative conditions.

Study Limitations

1
Compromised motor function may have influenced the MWM results.
2
ERG response may not fully capture the impact of LBE on retinal function.
3
Inconsistencies were noted across various regions such as the hippocampus, cortex, spinal cord, and retina

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