Recently researchers have provided very interesting evidence that a form of vitamin B3, called Nicotinamide Riboside, may have beneficial effects for Parkinson’s (PD). Their data suggests that nicotinamide riboside was able to rescue problems in mitochondria – the power stations of cells – in human cell-based models of Parkinson’s. And the results also suggest that this treatment could prevent the neurodegeneration of dopamine producing neurons.

Mitochondrial dysfunction is a key cellular process implicated in Parkinson’s, the most common genetic risk for which are mutations in b-Glucocerebrosidase (GBA), an enzyme required for the appropriate degradation of cellular waste products. Its activity is reduced both in genetic carriers of PD as well as individuals with idiopathic PD.

A series of experiments led by Michela Deleidi at the University of Tubingen, has directly tapped into the link between GBA and mitochondrial dysfunction. They addressed the effects of nicotinamide riboside, which is necessary for mitochondrial function and energy production on neuronal function and survival.

Nicotinamide riboside stimulated the production of new mitochondria in patient-derived neurons. These results were extended in a fly model, in which dietary supplementation with nicotinamide riboside reduced dopamine neuron loss and prevented motor decline compared to normal food alone.

This is encouraging news as over the last few years we have been exploring ways to bring nicotinamide riboside into trial to evaluate it as a potentially disease-modifying treatment for Parkinson’s via our Linked Clinical Trials programme.

Dr Richard Wyse, head of research and development, CPT.

Given its high bioavailability, good tolerability and ability to cross the blood brain barrier, these findings strongly support the potential of nicotinamide riboside in disease modification for Parkinson’s.

Read the full article here

The NAD+ Precursor Nicotinamide Riboside Rescues Mitochondrial Defects and Neuronal Loss in iPSC and Fly Models of Parkinson’s Disease - Michela Deleidi et al.