Niacin May Help Treat Early-onset Parkinson's Disease

Unhealthy mitochondria, one main cause of Parkinson’s disease due to hereditary reasons can be treated with Vitamin D3 or niacin.

Highlights

Niacin boosts levels of NAD compound in body for energy generation and DNA repair, which is critical for keeping mitochondria in shape and Parkinson's at bay.
Familial //forms of Parkinson's disease (PD) caused by mutations in PINK1 are linked to mitochondrial impairment.
The co-enzyme nicotinamide adenine dinucleotide (NAD+) is essential for both generating energy in mitochondria and nuclear DNA repair.
A diet supplemented with the NAD+ precursor nicotinamide rescued mitochondrial defects and protected neurons from degeneration.

People with certain forms of early-onset Parkinson's disease may benefit from boosting the amount of niacin in their diet, according to new research from the University of Leicester.

Niacin, or Vitamin B3, is found in a variety of foods, including nuts and meat. The team from the MRC Toxicology Unit at the University of Leicester studied fruit flies with a mutation that mimics Parkinson’s disease in humans.

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‘Drugs that block NAD-consuming DNA repair already exist to treat cancer,therefore these drugs could be repurposed to protect faulty mitochondria in Parkinson's disease.’

"This study strengthens the therapeutic potential for Vitamin B3/niacin-based dietary interventions in the treatment of Parkinson's disease" - Dr Miguel Martins, MRC Toxicology Unit, University of Leicester.

The results of the study, reveal a mechanism for how early-onset Parkinson's affects the brain, and point to other drugs that may also help this subset of patients.

Dr Miguel Martins, who led the study, explained, "Parkinson's disease occurs when dopaminergic neurons in a part of the brain called the substantia nigra are lost. This can happen for a variety of reasons, but in some hereditary cases, the main problem is unhealthy mitochondria - the organelles that power the cell.”

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"Mutations in genes such as PINK1 prevent cells from clearing out the defective powerhouses. When they accumulate, neurons can't get enough energy and die. The faulty mitochondria also release toxic molecules that damage their genes encoded by DNA.

NAD or nicotinamide adenine dinucleotide, a precursor of niacin is important for both energy generation and DNA repair. The team fed fruit flies with the mutated PINK1 gene food supplemented with niacin, which is made into NAD inside the body.

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The flies had far fewer faulty mitochondria than their mutant peers on a regular diet with this extra source of NAD.The vitamin also prevented the flies from losing neurons.

The team of neuroscientists then examined whether stopping DNA repair from depleting NAD would protect the flies with Parkinson's - and found that genetically switching this function off kept mitochondria healthy and neurons alive, as well as improved the flies' strength, mobility and lifespan.

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Dr Martins added: "The results suggest that in familial Parkinson's, available NAD is critical for keeping mitochondria in shape and the disease at bay. Drugs that block NAD-consuming DNA repair already exist to treat cancer. Loading up on niacin probably can't hurt either.

"While neither of these would be cures, they would expand treatment options for Parkinson's patients with faulty mitochondria. "This study strengthens the therapeutic potential for Vitamin B3/niacin-based dietary interventions and PARP inhibition in the treatment of Parkinson's disease."

Reference

Miguel Martins, Enhancing NAD+ salvage metabolism is neuroprotective in a PINK1 model of Parkinson's disease, Open Biology (2016) http://dx.doi.org/10.1242/bio.022186.

Source-Medindia