Manganese-induced Parkinsonism: Taurine as an Adjunctive Treatment?

David Quig, PhD | September 14, 2021

Parkinsonism is the most prevalent neurodegenerative disease affecting the motor system. There are different forms of Parkinsonism, but most patients are diagnosed with idiopathic Parkinson's disease at an average age of 60. Environmental factors may be involved; exposure to pesticides, and manganese dyshomeostasis have been implicated. Albeit relatively rare, manganism should be considered, especially for patients with compromised hepatic function. Manganese-induced Parkinsonism (MIP) will be reviewed, and recent preclinical research regarding the use of taurine as a potential treatment option for MIP will be highlighted.

The neuropathy of Parkinsonism is associated with the presence of intraneuronal fibrillar deposits of α-synuclein (Lewy bodies or Lewy neurites), and dysfunction of the dopaminergic system in specific regions of the brain. Oxidative stress/damage and mitochondrial dysfunction are pathologically involved, but there are currently no effective treatments for Parkinsonism.

Manganism is associated with excess retention of pro-oxidative Mn in specific regions of the brain, and deposition of Mn in brain is associated with liver diseases such as cirrhosis. MIP has phenotypic characteristics analogous to idiopathic Parkinsonism with a few distinct differences. Excess Mn adversely affects mitochondrial function, dopaminergic neurons, and the metabolism of monoaminergic neurotransmitters in the CNS. Manganism is most common with occupational exposure to airborne Mn, but it may occur with normal Mn exposure if the hepatobiliary excretion of Mn is diminished. Mn homeostasis is effectuated by low oral absorption (1-5%), and biliary-fecal excretion (98%). A demonstrative case of MIP involved a young child with normal Mn exposure and end stage hepatic failure. Parkinsonism symptoms and functional neuroimaging (SPECT) of her brain were similar to that of Mn miners, and the levels of Mn in hair, whole blood and urine were very high. Atypically, the child had significant recovery shortly after a liver transplant.

There are no effective noninvasive treatments for MIP, but some case reports of adults with MIP are suggestive of positive prognosis with extensive high-dose IV treatment with para-aminosalicylic acid (PAS). PAS, an old anti-tuberculosis drug, has been shown to enhance Mn decorporation and decrease brain Mn levels (animal models). PAS is not available in the U.S. for IV administration, and efforts have been made towards an oral sustained release, high load PAS delivery system.

Short of enhancing Mn decorporation from the CNS, recent research indicates that supplemental taurine (50-100 mg/kg) provides neuroprotective, mitochondria protective, and anti-oxidative effects in rodent models of MIP. Taurine ameliorated Mn-induced locomotor deficits, lowered brain levels of biomarkers of oxidative stress, and preserved mitochondrial function and integrity in brain tissue. Taurine also improved spatial learning and memory abilities. Further, via direct assessment, Mn alters the extracellular levels and metabolism of taurine and GABA in the striata of rats; those effects appear to be mediated by direct impact of Mn on the cellular transporters of the neurotransmitters. Clinical trials with taurine in occupationally exposed and MIP patients are needed.

One might consider assessment of Mn in whole blood for patients diagnosed with idiopathic Parkinsonism; high Mn levels warrant assessment of hepatobiliary function. Given the array of protective effects imparted by taurine, direct assessment of taurine status (plasma) may help guide intervention strategies for patients suffering from Mn-induced Parkinsonism.



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