# Progress and Prospects in Parkinson's Research/Therapy/Neuroprotection/Vitamin D
## Background

Vitamin D was isolated by an American researcher, Elmer McCollum in 1921. He called it Vitamin D because it was the fourth such compound to be identified. Nutritionally it is found in fish (particularly salmon and tuna) and in dairy products. Vitamin D3 is also uniquely synthesised by the action of ultra-violet rays from sunlight on the skin.

## Research

2001
Wang et al induced PD in rats after first treating them with enhanced levels of vitamin D3.http://www.ncbi.nlm.nih.gov/pubmed?term=wang%20vitamin%20D%20hoffer%202001
   Taken together, our data indicate that D3 pretreatment attenuates the hypokinesia and DA neuronal toxicity induced by 6-OHDA.
2006
Smith et al evaluated the potential benefits of calcitriol in the treatment of PD. This is the hormonally active form of vitamin D and it has been implicated as an agent that has neuroprotective effects in various animal models of diseases, possibly by upregulating GDNF (q.v.). Parkinsonism was invoked in rats by the administration of 6-OHDA, and these were then treated with calcitriol. . It was found that GDNF was significantly increased in the substantia nigra, but not in the striatum.
   These results suggest that long-term treatment with calcitriol can provide partial protection for dopaminergic neurons against the effects of intraventricularly administered 6-OHDA.
2011
Butler et alexamined a large cohort of PD patients with a view to establishing genetic links to Vitamin D receptors, Their conclusions state:-
   Our findings suggest VDR as a potential susceptibility gene and support an essential role of vitamin D in PD.
2012
Luong and Nguyễn argue the case for Vitamin D’s therapeutic properties in the treatment of PD and evaluate the following genomic factors in this context:-
* Major Histocompatibility Complex (MHC);
* VDR and 1α-hydroxylase;
* The Cytochrome P$_{450}$ (CYP);
* The Renin-Angiotensin System (RAS);
* Poly(ADP-Ribose) Polymerase-1 (PARP-1);
* Neurotrophic Factors (NTFs);
* Heme Oxygenase-1 (HO-1);
* Sp1 Transcription Factor.
together with the following non-genomic factors:-
* Diabetes Mellitus (DM);
* L-Type Voltage-Sensitive Calcium Channels (L-VSCC);
* Nerve Growth Factor (NGF);
* Matrix Metalloproteinases (MMPs);
* Prostaglandins (PGs);
* Oxidative Stress;
* Nitric Oxide Synthase (NOS).

## Further Reading

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## Related pages

Therapy > Neuroprotection
Sub Pages:
    Neuroprotective agents
    Substances with possible neuroprotective properties:
    Caffeine,--Celastrol,--Co-Enzyme Q10,--Creatine,--DHA,--Exendin-4 (EX-4),--GDNF,--Glutathione (GSH),--GM1,--Isradipine,--Melatonin,--Minocycline,--Nicotine,--NSAIDs,--Phenylbutyrate,--Phytic Acid,--Probucol,--Quinoxaline,--Rasagiline,--Riboflavin,--Statins,--Tolcapone,--Urate & Uric Acid,--Vitamin D,--Vitamin E,--
See also: Vitamin D deficiency