A specific form of magnesium taken orally and able to readily enter the brain was seen to ease Parkinson’s-related motor problems and nerve cell loss in a mouse model of the disorder.
The study, “Treatment Of Magnesium-L-Threonate Elevates The Magnesium Level In The Cerebrospinal Fluid And Attenuates Motor Deficits And Dopamine Neuron Loss In A Mouse Model Of Parkinson’s disease,” was published in Neuropsychiatric Disease and Treatment.
Magnesium is a mineral important to several body functions, including nerve cell transmission and neuromuscular coordination. Low levels of this mineral have been reported in motor regions of the brains of Parkinson’s patients. Population studies of the disease (epidemiological studies) also report a higher incidence of the neurodegenerative disorder in the presence of magnesium deficiency.
Therefore, in theory, raising brain magnesium levels could ease Parkinson’s manifestations.
Magnesium sulfate is the first choice as a clinical magnesium supplement, but systemic administration of magnesium sulfate fails to increase magnesium levels in the cerebrospinal fluid (CSF), the liquid that flows in and around the brain and spinal cord.
Using a mouse model of Parkinson’s, researchers investigated the protective effect of magnesium-L-threonate, a magnesium compound that is very permeable and can penetrate the blood-brain barrier — a semipermeable membrane that protects the brain from the outside environment — to reach the brain.
For a month, animals were given one of three doses of magnesium-L-threonate (0.8, 1.2, and 1.6 mM) or magnesium sulfate in their drinking water. Then, on the third week of the magnesium regimen, and for 7 seven consecutive days, these mice received MPTP, a neurotoxin that induces death of dopamine-producing neurons and mimics Parkinson’s symptoms.
Scientists analyzed the animals’ motor behavior and the amount of nerve cell loss within the substantia nigra and the striatum, both motor control brain areas primarily affected by Parkinson’s.
Magnesium levels in blood serum and the cerebrospinal fluid were measured after either form of oral magnesium in healthy mice.
Magnesium concentrations in both the CSF and serum rose with magnesium-L-threonate use, while magnesium sulfate only increased blood magnesium levels and did not affect CSF levels.
Diseased mice with Parkinson’s-like symptoms given magnesium-L-threonate for four weeks were seen to have lesser motor decline and better motor coordination compared to untreated diseased mice. Treatment also slowed dopaminergic neuronal loss in a dose-dependent manner, with the 1.2 mM dose showing the greatest neuroprotective potential.
Additionally, magnesium-L-threonate treatment inhibited what’s called inducible nitric oxide synthase (iNOS)-mediated inflammation and oxidative stress. (Oxidative stress refers to cellular damage as a consequence of high levels of oxidant molecules and is associated with a number of diseases, including Parkinson’s.)
Treatment with magnesium sulfate had a marginal effect on the animals’ motor behavior, but no effect on neurodegeneration.
“[O]ur results indicate MgT [magnesium-L-threonate] can significantly attenuate MPTP-induced motor deficits and DA [dopaminergic] neuron injury, which may be related to its ability of increasing the Mg [magnesium] concentration in the CSF [cerebrospinal fluid],” the researchers wrote.
“These data also suggest that … only supplementation of [magnesium] in the periphery does not help to protect the brain and the combination of [magnesium] with an agent that promotes its transportation to the brain is essential for the neuroprotection of this element,” they added.