Protection of multiple aspects of Alzheimer’s disease pathology using dietary supplementation with taurine

TL;DR

This study shows that taurine supplementation can protect against Alzheimer's disease pathology in mice, offering a potential dietary strategy for prevention.

Contribution

The study demonstrates that taurine can mitigate multiple aspects of Alzheimer's pathology in mice through both acute and long-term administration.

Findings

Taurine at 2000 mg/kg/day reduced neuroinflammation and protected the dentate gyrus in older mice.

Taurine supplementation for 1–2 months led to a small reduction in Aβ42 burden in older mice.

Taurine altered key metabolites in AD-affected brain regions, moving them closer to wild-type profiles.

Abstract

As Alzheimer’s disease (AD) continues to rise amongst the aging population, preventative measures such as dietary or lifestyle changes represent an attractive option to mitigate the burden. Taurine, known for its antioxidant and anti-inflammatory properties, may also play a neuroprotective role. This study investigates the protective effects of taurine supplementation in 5xFAD mice. Taurine was administered through drinking water at doses of 0, 500, 1000, 2000, 4000 mg/kg/day, with no change in water consumption or body mass was observed. Postmortem markers of neuroinflammation using cytokine profiling demonstrated that 2000 mg/kg/day was effective at invoking a protective response against AD progression. An acute dose of this concentration, in older mice, was also sufficient at protecting the dentate gyrus against gliosis and preventing volume loss. Supplementation of taurine for 1–2 months in older mice also led to a small, reduction in the Aβ42 burden. This suggests that both long-term and acute administration of taurine can mitigate pathological characteristics of AD. High-resolution magic angle spinning magnetic resonance spectroscopy (HRMAS-MRS) was used to analyze and differentiate the molecular profile of 3 key AD-affected regions: frontal cortex, ventral and dorsal hippocampus. Significant changes in 5 metabolites (GABA, glutamate, NAA, aspartate and scyllo-inositol) were observed in AD at two different ages (3–4 months and 8 months). Taurine moved a number of metabolites including NAA and glutamate closer to the wild-type profile consistent with neuroprotection. Overall, these findings support dietary taurine supplementation as a promising preventative strategy for AD.

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