Forking off the other thread, I would like to know if anyone is looking at ways of persuading one's own brain to produce its own GDNF? Seems obvious but thought I would ask. Anyone know?

But it looks like something someone should be looking into.


1: Biosci Biotechnol Biochem. 2005 Apr;69(4):800-5.

Oral administration of royal jelly facilitates mRNA expression of glial cell
line-derived neurotrophic factor and neurofilament H in the hippocampus of the
adult mouse brain.

Hashimoto M, Kanda M, Ikeno K, Hayashi Y, Nakamura T, Ogawa Y, Fukumitsu H,
Nomoto H, Furukawa S.

Laboratory of Molecular Biology, Gifu Pharmaceutical University, Gifu 502-8585,
Japan.

Royal jelly (RJ) is known to have a variety of biological activities toward
various types of cells and tissues of animal models, but nothing is known about
its effect on brain functions. Hence, we examined the effect of oral
administration of RJ on the mRNA expression of various neurotrophic factors,
their receptors, and neural cell markers in the mouse brain. Our results revealed
that RJ selectively facilitates the mRNA expression of glial cell line-derived
neurotrophic factor (GDNF), a potent neurotrophic factor acting in the brain, and
neurofilament H, a specific marker predominantly found in neuronal axons, in the
adult mouse hippocampus. These observations suggest that RJ shows neurotrophic
effects on the mature brain via stimulation of GDNF production, and that enhanced
expression of neurofilament H mRNA is involved in events subsequently caused by
GDNF. RJ may play neurotrophic and/or neuroprotective roles in the adult brain
through GDNF.

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

Rick,
I just deleted what I had and left the cogane, thinking that you are asking about something you could possibly do yourself. I do not know if or how you could get this substance.

http://www.phytopharm.com/portfolio/?id=2234

paula

I take Royal Jelly but sometimes I wonder if I am just pissing in the wind. I am interested in stimulating production of GDNF. I must confess I know very little about GDNF or the fiasco. I think I remember it showed promise but was yanked.

.....here's the story, smithclayriley.

http://pdpipeline.org/advocacy/gdnf_table.htm

paula

Dr. Bronstein talked about a growth factor-like drug, that was currently in trials. It sounded promising. I will ask him about it.
Charlie

http://www.biomedcentral.com/1471-2202/5/41/abstract

Research article
Neural stem cells express melatonin receptors and neurotrophic factors: colocalization of the MT1 receptor with neuronal and glial markers
Lennard P Niles1 , Kristen J Armstrong1 , Lyda M Rincón Castro1 , Chung V Dao1 , Rohita Sharma1 , Catherine R McMillan1 , Laurie C Doering2 and David L Kirkham2

1Department of Psychiatry and Behavioural Neurosciences, McMaster University 1200 Main Street West, Hamilton ON L8N 3Z5, Canada

2Department of Pathology and Molecular Medicine, McMaster University 1200 Main Street West, Hamilton ON L8N 3Z5, Canada

author email corresponding author email

BMC Neuroscience 2004, 5:41doi:10.1186/1471-2202-5-41


Published: 28 October 2004

Abstract
Background
In order to optimize the potential benefits of neural stem cell (NSC) transplantation for the treatment of neurodegenerative disorders, it is necessary to understand their biological characteristics. Although neurotrophin transduction strategies are promising, alternative approaches such as the modulation of intrinsic neurotrophin expression by NSCs, could also be beneficial. Therefore, utilizing the C17.2 neural stem cell line, we have examined the expression of selected neurotrophic factors under different in vitro conditions. In view of recent evidence suggesting a role for the pineal hormone melatonin in vertebrate development, it was also of interest to determine whether its G protein-coupled MT1 and MT2 receptors are expressed in NSCs.

Results
RT-PCR analysis revealed robust expression of glial cell-line derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in undifferentiated cells maintained for two days in culture. After one week, differentiating cells continued to exhibit high expression of BDNF and NGF, but GDNF expression was lower or absent, depending on the culture conditions utilized. Melatonin MT1 receptor mRNA was detected in NSCs maintained for two days in culture, but the MT2 receptor was not seen. An immature MT1 receptor of about 30 kDa was detected by western blotting in NSCs cultured for two days, whereas a mature receptor of about 40 – 45 kDa was present in cells maintained for longer periods. Immunocytochemical studies demonstrated that the MT1 receptor is expressed in both neural (β-tubulin III positive) and glial (GFAP positive) progenitor cells. An examination of the effects of melatonin on neurotrophin expression revealed that low physiological concentrations of this hormone caused a significant induction of GDNF mRNA expression in NSCs following treatment for 24 hours.

Conclusions
The phenotypic characteristics of C17.2 cells suggest that they are a heterogeneous population of NSCs including both neural and glial progenitors, as observed under the cell culture conditions used in this study. These NSCs have an intrinsic ability to express neurotrophic factors, with an apparent suppression of GDNF expression after several days in culture. The detection of melatonin receptors in neural stem/progenitor cells suggests involvement of this pleiotropic hormone in mammalian neurodevelopment. Moreover, the ability of melatonin to induce GDNF expression in C17.2 cells supports a functional role for the MT1 receptor expressed in these NSCs. In view of the potency of GDNF in promoting the survival of dopaminergic neurons, these novel findings have implications for the utilization of melatonin in neuroprotective strategies, especially in Parkinson's disease.