A 2026 study concludes that lutein is a strategy for treating Parkinsons. This particular study uses animals – in this case mice. Obviously, results may not translate to humans, but animal studies often are replicated in studies using human subjects. Lutein is often recommended as a supplement to benefit problematic eye conditions.

It is a natural supplement that requires no prescription from a doctor, so this natural option is readily available to give a trial spin. Will taking lutein be a beneficial treatment for you? As with all natural therapies it will likely be beneficial to some but not others. The cost of experimentation is small compared to the potential benefit, so why not consider this as an option to be investigated further?

Robert Rodgers PhD
Founder 2004
Parkinsons Recovery
Road to Recovery from Parkinsons Disease

Study Concludes Lutein is a Strategy for Treating Parkinsons

J Integr Neurosci. 2026 Jan 23;25(1):45758. Lutein Attenuates Parkinson’s Disease Progression by Regulating Mitochondrial Function via the TRIM31/Drp1 Signaling Pathway

Abstract

Background: Mitochondrial dysfunction is closely associated with the pathogenesis of Parkinson’s disease (PD). Lutein has been shown to exert protective effects in neurological disorders. This study aimed to investigate the ameliorative effects of lutein on mitochondrial function in PD and its underlying molecular mechanisms.

Methods: Animal and cellular PD models were established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice and treatment of SH-SY5Y cells with 1-methyl-4-phenylpyridinium ion (MPP+), respectively. Motor function was assessed using the rotarod, adhesive removal, and pole tests. Mitochondrial function was evaluated using MitoSOX Red staining, JC-1 staining, and adenosine triphosphate (ATP) content measurement. Western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to measure the levels of relevant proteins and mRNA.

Results: Lutein significantly ameliorated MPTP-induced motor dysfunction in PD mice, increased the number of tyrosine hydroxylase (TH)-positive neurons, and alleviated damage to striatal brain tissue. At the cellular level, lutein significantly suppressed MPP+-induced apoptosis of SH-SY5Y cells, upregulated the expression of B-cell lymphoma-2 (Bcl-2), and downregulated the expression of Bcl-2-associated X protein (Bax) and cleaved caspase-3.

Additionally, lutein significantly reduced reactive oxygen species (ROS) levels, restored mitochondrial membrane potential, increased ATP levels, and increased the activity of mitochondrial respiratory chain complex I. At the molecular level, lutein promoted the ubiquitination of dynamin-related protein 1 (Drp1), whose degradation was impaired in the PD model. This effect was mediated by the E3 ubiquitin ligase Tripartite Motif-containing protein 31 (TRIM31), whose expression was downregulated in the disease state. Functional experiments confirmed that overexpression of TRIM31 enhanced Drp1 ubiquitination and improved mitochondrial function, whereas TRIM31 knockdown partially attenuated the therapeutic effects of lutein.

Conclusion: In summary, this study revealed, for the first time, that lutein alleviates PD progression by increasing Drp1 ubiquitination and degradation via TRIM31 transcription and translation, ultimately improving neuronal mitochondrial function. These findings not only elucidate a novel mechanism underlying lutein’s neuroprotective effect but also identify a potential therapeutic target and offer a new strategy for PD treatment.