Science Update

Recent Review Explores Relationship Between Certain Micronutrients and Mitochondrial Dysfunction in Neurodegeneration

Mitochondria, the ‘powerhouse of the cell,’ are essential for energy production and many other biochemical processes in the body. Dysfunctions in mitochondria can impact every organ system in the body. 

Recent research indicates that mitochondrial dysfunction may play a role in neurodegenerative diseases such as Parkinson’s Disease (PD) and Alzheimer’s Disease (AD). The pathophysiology is thought to be attributed to a potentially reduced capacity for adenosine triphosphate (ATP) production and other biochemical changes. Mitochondrial dysfunction has been observed in toxin-induced PD models and genetic and sporadic forms of PD. Reduced ATP levels in platelets and fibroblasts, altered mitochondrial morphology, and decreases in mitochondrial complex IV activity have been observed in AD. Disruptions in mitochondrial structure and function have also been observed in amyotrophic lateral sclerosis (ALS). 

A recently published review article by Mantle and colleagues explored the potential relationship between certain micronutrients and mitochondrial dysfunction in neurodegenerative diseases. The authors reported that there were certain nutrient deficiencies in the presence of neurodegenerative disorders, including coenzyme Q10 (CoQ10), selenium, certain B vitamins, and vitamin D3 (cholecalciferol). 

Mantle and colleagues describe studies that link supplementation of certain micronutrients with potential benefits in neurodegenerative disorders. A phase II clinical trial explored the potential efficacy of oral CoQ10 supplementation in the presence of PD. It reported an attenuation of the functional decline associated with early-stage PD. A contrasting study was also described; however, the authors note that deficiencies in CoQ10 were not assessed, and this may contribute to the reported limited therapeutic potential of CoQ10 supplementation in PD.

In an animal study, selenium supplementation was shown to help modulate impaired dopaminergic neurotransmission in PD mouse models. In human populations, selenium, in combination with certain probiotics, was shown to help improve parameters related to cognitive function. Another clinical trial reported improvements in Mini-Mental State scores in patients with AD in the presence of high-dose selenate. 

In a clinical trial involving 50 participants with PD, long-term supplementation with intramuscular vitamin B1 (thiamin) was shown to help improve motor function and other certain PD-related symptoms. In another clinical trial, oral supplementation with vitamin B2 for six months was shown to improve parameters related to motor function in individuals with PD.

In a randomized controlled trial, supplementation with a combination of alpha-lipoic acid (ALA) and Ω-3 fatty acids for twelve months was shown to help slow functional and cognitive decline in individuals with AD. Slowed disease progression in individuals with mild dementia was reported in an open-label clinical study involving 600 mg ALA daily for 48 months in 43 individuals with AD. Other clinical studies showed that supplementation with vitamin D3 helped reduce the risk of osteopenia in individuals with PD and may have helped improve cognitive decline in patients with AD. 

The authors conclude that certain micronutrients may help support parameters related to neurodegenerative diseases. While more clinical studies are needed before conclusions can be made, research indicates certain vitamins, minerals (e.g., selenium), and micronutrients may help support cognitive function and brain health.

By Colleen Ambrose, ND, MAT