A Case of Parkinson’s Disease Symptom Reduction with Intravenous NAD +
Erin Gadol 1*, Richard F. Mestayer 1,2, Ross Grant 3,4, Yevgeniy Grigoryev 5, Susan B.
Gibson 6, and Michael Happel 7
1 NAD Research, Incorporated, USA
2 Springfield Wellness Center, USA
3 Australasian Research Institute, Australia
4 Department of Pharmacology, School of Medical Sciences, University of New South Wales, Australia
5 Department of Biology, City College of New York, USA
6 School of Natural and Behavioral Sciences, William Carey University, United States
7 Northlake Neurological Institute, United States
*Corresponding authors: Erin Gadol, NAD Research, Incorporated, 32900 Pitcher Road, Springfield, LA 70462 USA, Tel: +1 917-771-7576; Fax: +1 225-294-5944; E-mail: email@example.com
Received: March 02, 2019; Accepted: March 28, 2019; Published: April 05, 2019
Copyright: ©2019 Gadol E, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Citation: Gadol E, Mestayer RF, Grant R, Grigoryev Y, Gibson SB, et al. (2019) A Case of Parkinson’s Disease Symptom Reduction with Intravenous NAD+. Case Rep Lit Rev 3(1): 100021.
Keywords: Parkinson’s disease, neurodegeneration, NAD+
The reduction in PD symptoms this patient experienced during initial treatment, including the eventual discontinuation of anti-PD medication, lends significant anecdotal support for the use of NAD+ as a potentially useful treatment for at least a subset of Parkinson’s disease patients. Although the biochemical processes involved in PD pathogenesis are complex and varying between cases, the association between increased oxidative damage and reduced NAD+ availability in the pathobiochemistry of neurodegenerative disease provide at least some rationale for the marked symptom reduction in this case [7,8]. Additionally, as prior research suggests, increasing the availability of NAD+ to dopaminergic neurons in the nigrostriatal tracts may have the potential to promote healthy mitochondrial function and DNA repair. Moreover, in a murine model, NAD+supplementation has demonstrated neuronal restoration following the induction of neurodegeneration [9,10]. Furthermore, one recent study has directly linked NAD+ precursor administration to preventing dopaminergic neuronal loss in PD patient derived induced pluripotent stem cells . Overall, our current study supports the notion that NAD+ supplementation may be increasing cellular resilience to ongoing dopaminergic neuronal loss in this particular PD sufferer.
Although the evidence obtained from observations reported for this single individual does not claim that NAD+ targets disease pathogenesis, the significant clinical improvements indicate that NAD+ therapy can alleviate symptoms in at least a subset of PD sufferers. These extraordinary observations warrant further clinical investigation of NAD+ and its potential to modulate key cellular processes impaired in neurodegenerative diseases such as PD.