Posted 23 February 2014 - 01:52 AM
Edited by Flex, 23 February 2014 - 02:21 AM.
Posted 23 February 2014 - 02:04 AM
Edited by Flex, 23 February 2014 - 02:19 AM.
Posted 23 February 2014 - 05:53 AM
Edited by LexLux, 23 February 2014 - 06:29 AM.
Posted 23 February 2014 - 06:56 AM
Posted 23 February 2014 - 10:01 AM
Edited by Flex, 23 February 2014 - 10:34 AM.
Posted 23 February 2014 - 02:06 PM
Posted 23 February 2014 - 07:09 PM
Edited by Flex, 23 February 2014 - 07:30 PM.
Posted 28 February 2014 - 03:52 PM
Posted 28 February 2014 - 04:13 PM
Ultimately, another study that shows that scientific experiments which pump lots of chemicals into monkeys are bad for monkey health.It is also worth noting that, because of the relatively small volume of CSF in monkeys, all doses used in this toxicology study would likely be associated with CSF concentrations far higher than in humans.
Posted 28 February 2014 - 06:53 PM
Posted 02 March 2014 - 12:20 AM
Thx :-)
Uridine and DHA
Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides
http://www.ncbi.nlm....pubmed/19262950
As far as I remember I read the fulltext where they mentioned the usage of Uridine 5´-momophosphate disodium salt
Posted 16 March 2014 - 10:21 PM
So taking into consideration the slight cancer concern, my intuition is to dose on a one week on/one week off schedule, maybe after a four week 'attack' phase. Thoughts?
So I have spent most of the morning reading about NGF, BDNF, interaction with cancers and supplements/nutrients. I'm not convinced that there is an actual increase in getting any form of cancer from boosting NGF/BDNF by itself. Let me try to breakdown what I've manage to gather.
In cancer tumors elevated levels of NGF has been found and is known to be one of the factors that benefit the tumor in it's growth. Medication suppressing NGF in this case can be benificial for the treatment of the growth of the tumor. NGF is something that is naturally increased in areas where there is inflammation in order to help the body to repair the area. Inflammation is something that is the effect of all age related damage and diseases. In cancer models NFG is malfunctioning since the body can not separate the mutated cells from healthy ones, hence cancers cells growth and survivability is also enhanced since the body is repairing it. This is my understanding of what goes on with NGF in a cancer model.
There is a great article here that explains the real effect of antidepressants in the brain/body and also talks about BDNF in repairing inflammation in the brain (all backed with studies):
http://www.wellnessr...arly_mortality/
From looking at research on Lion's Mane the mushroom does increase NGF/BDNF levels. There is a bunch of other things that work on NGF/BDNF as well including common nutrients like blueberries and cucumin. Lion's Mane is proven anti-inflammatory and with other cancer benefits so the notion that it would increase risk for cancer sounds highly improbable to me. There is no studies that show anything like this with Lion's Mane and either with other natural NGF/BDNF modulators that I have been able to find. NGF/BDNF does not cause any cells to mutate into cancer cells, it might however not be beneficial if you already have cancer.
And to finish it all off, exercise has been shown to increase NFG and BDNF levels as well. Does that mean exercise causes cancer? No... There is a lot more to this than that. My personal opinion is that it's not probable and I will be adding Lion's Mane to my stack in the future.
Some more interesting stuff here on mental health and BDNF: http://samsnyder.com...ncreasing-bdnf/Medications:
1. Ketamine use, which has rapid antidepressant properties, is associated with elevated levels of BDNF. (Link)
2. Memantine, which has antidepressant properties, elevates levels of BDNF. (Link)
3. Agomelatine increases hippocampal BDNF and has antidepressant properties. (Link)
4. Riluzole restores hippocampal BDNF expression and has antidepressant properties. (Link)
5. Escitalopram is an antidepressant that reverses BDNF deficits. (Link)
6. Atypical antipsychotics increase BDNF levels and have antidepressant effects. (Link)
7. Venlafaxine is an antidepressant that increases BDNF levels. (Link)
8. Olanzapine increases BDNF levels and augments antidepressant treatment. (Link)
9. Lithium upregulates BDNF and treats bipolar disorder. (Link)
10. Sertraline is an antidepressant that increases BDNF. (Link)
11. Risperidone increases BDNF levels and augments antidepressant treatment. (Link)
12. Imipramine is an antidepressant that up-regulates BDNF expression. (Link)
13. Mirtazapine is an antidepressant that increases BDNF gene expression. (Link)
14. Metyrapone enhances BDNF gene expression and has antidepressant properties. (Link)
15. Rolipram normalizes BDNF levels and has antidepressant properties. (Link)
Other Psychiatric Treatments:
1. Repetitive transcranial magnetic stimulation increases BDNF levels and has antidepressant effects. (Link)
2. Electroconvulsive therapy elevates BDNF levels and has antidepressant effects. (Link)
3. Vagal nerve stimulation activates BDNF receptors and treats depression. (Link)
Food and Lifestyle:
1. A Mediterranean diet increases BDNF levels in depressed patients. (Link)
2. Green odor elevates BDNF and has antidepressant properties. (Link)
3. Music enhances BDNF levels and improves mood. (Link)
4. Alpha-linolenic acid increases BDNF and reduces depressive behavior. (Link)
Supplements:
1. Fish oil has antidepressant effects that involve BDNF. (Link)
2. Ginsenoside prevents a stress-induced reduction in BDNF levels. (Link)
3. Hyperoside has antidepressant properties and elevates BDNF expression. (Link)
4. Magnolol restores BDNF expression and has antidepressant effects. (Link)
5. Curcumin reverses a decrease in BDNF levels and produces an antidepressant effect. (Link)
6. Zinc increases the BDNF mRNA level and has antidepressant effects. (Link)
7. Beta-alanine increases BDNF concentration and has anti-anxiety properties. (Link)
8. Flavonols enhance BDNF expression and have antidepressant properties. (Link)
9. Suyu-Jiaonang attenuates a reduction in BDNF and has antidepressant properties. (Link)
10. Ferulic acid increases BDNF mRNA and ameliorates stress-induced depressive behavior. (Link)
11. Nicotine increases BDNF levels and has antidepressant properties. (Link)
12. Polygala tenuifolia increases BDNF expression and has antidepressant effects. (Link)
13. Xiaoyaosan reverses decreases in BDNF and has antidepressant effects. (Link)
14. Piperine reverses the reduction in BDNF and has antidepressant properties. (Link)
15. Danzhi Xiaoyao powder increases BDNF levels and reduces depressive symptoms. (Link)
16. Ginkgo biloba extract increases BDNF expression and reduces the effects of stress. (Link)
17. Eugenol has antidepressant activity and induces BDNF. (Link)
Posted 16 March 2014 - 10:35 PM
GDNF family receptor complexes are emerging drug targets :"GDNF protects and repairs dopamine-containing neurons, which degenerate in Parkinson's disease, and motoneurons"
and this sounds very good for me considering I'm trying to reverse damages to my dopamine pathways induced by nicotine addiction.
Alcohol Reward, Dopamine Depletion, and GDNF:
"Barak et al. (2011), rats were given intermittent 24 h access to alcohol solutions three times a week for 7 weeks to develop alcohol dependence. Then NAc extracellular dopamine levels and its response to VTA GDNF injections were measured. The authors showed that NAc dopamine levels in alcohol-dependent rats were significantly decreased after 1 h of withdrawal and remained low 24 h later. VTA GDNF injections (10 μg/side) in 24-h-withdrawn rats restored NAc dopamine to control (normal) levels.
Next, the authors demonstrated that VTA GDNF injections have functional consequences on behavior. Injections of GDNF into VTA 10 min before pairing one chamber of a CPP apparatus with 0.5 g/kg alcohol (i.p.) during two conditioning sessions [interspersed with two pairings of saline (i.p.) in a contextually distinct chamber on the opposite side of the apparatus] prevented the development of CPP in alcohol-dependent rats. VTA GDNF injections given 10 min before a CPP test prevented the expression of CPP. Importantly, VTA injections of GDNF alone caused no preference or aversion. Finally, in alcohol-dependent rats trained to press a lever to receive alcohol (2.5–40%), VTA GDNF injections produced a downward shift in the dose–response curve. The rats made fewer responses and received fewer alcohol deliveries at each concentration tested on days when the rats received GDNF compared with days in which they received vehicle injections. Such downward shifts in the dose–response curve are usually interpreted as a decrease in the rewarding effect of the drug.
These results have several important implications for our understanding of GDNF's role in alcohol reward. First, these results extend the authors' previous results showing that VTA GDNF decreases alcohol intake and that heterozygous genetic knock-out of the GDNF gene increases rewarding effects of alcohol (Carnicella et al., 2009). The CPP findings extend the previous work with knock-out mice by showing that the role of GDNF in alcohol reward is localized, at least in part, to the VTA. Second, these findings demonstrate a role for GDNF both in acquisition and expression of the CPP memory.
Most relevant to the dopamine-depletion hypothesis is the finding that VTA GDNF injections normalized the decreased NAc dopamine levels during alcohol withdrawal and also decreased alcohol reward. This dual effect of GDNF injections provides one plausible explanation for the role of VTA GDNF in decreasing alcohol reward—reversing the dopamine depleted dysphoric state. However, these are correlative findings that are open to alternative interpretations. One such possibility is that GDNF acts in the VTA to decrease the rewarding effects of alcohol in a dopamine-independent manner. In this regard, there is evidence for dopamine-independent reward mechanisms in the VTA (Nader and van der Kooy, 1997; Ikemoto et al., 1998)."
Role for GDNF in Biochemical and Behavioral Adaptations to Drugs of Abuse:
"Abstract
The present study examined a role for GDNF in adaptations to drugs of abuse. Infusion of GDNF into the ventral tegmental area (VTA), a dopaminergic brain region important for addiction, blocks certain biochemical adaptations to chronic cocaine or morphine as well as the rewarding effects of cocaine. Conversely, responses to cocaine are enhanced in rats by intra-VTA infusion of an anti-GDNF antibody and in mice heterozygous for a null mutation in the GDNF gene. Chronic morphine or cocaine exposure decreases levels of phosphoRet, the protein kinase that mediates GDNF signaling, in the VTA. Together, these results suggest a feedback loop, whereby drugs of abuse decrease signaling through endogenous GDNF pathways in the VTA, which then increases the behavioral sensitivity to subsequent drug exposure.
[...]
The major objective of the present study was to assess such a role for one particular neurotrophic factor, GDNF (glial cell line–derived neurotrophic factor). We focused on GDNF for several reasons. First, GDNF enhances the survival and maintains the differentiated properties of dopaminergic neurons in cell culture and does so far more potently compared to BDNF and other neurotrophins (Lin et al. 1993). Second, GDNF dramatically enhances the survival of midbrain dopamine neurons in vivo after challenge with dopaminergic neurotoxins such as 6-hydroxydopamine or MPTP (2 and 23). GDNF also protects animals from the behavioral deficits associated with such lesions. Strikingly, a single injection of GDNF into the midbrain can exert such protective effects for at least one month (23 and 61). Third, signaling proteins for GDNF, GFRα1 and the associated protein tyrosine kinase Ret, are both highly enriched in midbrain dopamine neurons (55, 56, 57 and 58). The binding of GDNF to its receptor complex causes the phosphorylation and activation of Ret, which then mediates the physiological effects of the neurotrophic factor.
[...]
Discussion [MUST READ]
The major findings of this study are that exogenous GDNF, administered directly into the rat VTA, blunts both biochemical and behavioral adaptations to repeated administration of drugs of abuse. The study also establishes that endogenous GDNF systems are required for normal biochemical and behavioral responses to drug exposure: infusion of anti-GDNF antibody directly into the VTA increases a rat's sensitivity to drug effects, and mice that lack one copy of the GDNF gene show a similar increase in drug sensitivity. This is a particularly important observation because it extends what we know about the role of GDNF in the regulation of dopaminergic neurotransmission. Thus, research to date has only shown the pharmacological ability of exogenously applied GDNF to protect dopamine neurons in the adult brain in vivo from neurotoxic injury (see Introduction). The results of the present study implicate endogenous GDNF systems in regulating the function of adult dopamine neurons, in particular, regulating their responses to drugs of abuse. Moreover, based on our findings that chronic drug exposure decreases the phosphorylation of the GDNF signaling protein Ret in the VTA, we hypothesize further that some of the long-term effects of morphine and cocaine on the mesolimbic dopamine system are achieved via perturbation of endogenous GDNF signaling pathways.
[...] the fact that GDNF blocks behavioral responses to drug exposure means that the net effect of the neurotrophic factor must involve biochemical changes that oppose drug action.
The contrast between the effects of GDNF and BDNF on actions of drugs of abuse is interesting. Intra-VTA infusions of BDNF, like those of GDNF, in rats block some of the biochemical adaptations to morphine and cocaine, for example, induction of tyrosine hydroxylase in the VTA and of protein kinase A in the NAc (Berhow et al. 1995). Yet, a recent study showed that BDNF dramatically augments an animal's responses to the locomotor and rewarding properties of cocaine ( Horger et al. 1999). Such augmented behavioral responses would make sense if the biochemical adaptations blocked by BDNF are homeostatic; that is, they serve to reduce further drug effects. Presumably, these findings indicate that the net effect of BDNF, in contrast to that of GDNF, involves biochemical changes that increase behavioral responses to drug exposure. Consistent with this interpretation is the finding that BDNF knockout mice, in contrast to GDNF knockout mice, show reduced behavioral plasticity to repeated cocaine administration ( Horger et al. 1999). The biochemical endpoints examined in the present study and in the earlier studies of BDNF likely represent only a small portion of the adaptations that chronic drug administration causes in the VTA and NAc. Therefore, a major goal of future research is to further characterize the influence of GDNF and BDNF on the mesolimbic dopamine system, with the objective of finding differences in the molecular and cellular actions of the two neurotrophic factors that explain their opposite behavioral effects.
[...]
To conclude, the results of the present study establish a functional interaction between GDNF and drugs of abuse at the level of the mesolimbic dopamine system. The findings highlight the complex types of mechanisms that are likely induced in the brain by chronic exposure to a drug of abuse. The involvement of GDNF and perhaps other neurotrophic factor systems in drug-induced neural and behavioral plasticity could be particularly important for the very long-lived changes in brain function associated with addiction. These results also raise the interesting possibility that medications targeted to GDNF or to its signaling pathway could be useful as novel treatment agents for addictive disorders in humans."
Edited by LexLux, 16 March 2014 - 11:10 PM.
Posted 19 March 2014 - 01:51 AM
Posted 19 March 2014 - 12:54 PM
Edited by LexLux, 19 March 2014 - 12:54 PM.
Posted 19 March 2014 - 09:14 PM
Edited by Flex, 19 March 2014 - 09:18 PM.
Posted 20 March 2014 - 01:47 AM
Posted 20 March 2014 - 02:03 AM
Posted 20 March 2014 - 02:13 AM
Edited by Phoenicis, 20 March 2014 - 02:43 AM.
Posted 20 March 2014 - 02:34 AM
Edited by Flex, 20 March 2014 - 02:39 AM.
Posted 20 March 2014 - 02:59 AM
Edited by normalizing, 20 March 2014 - 03:00 AM.
Posted 20 March 2014 - 11:04 AM
Edited by OpaqueMind, 20 March 2014 - 11:08 AM.
Posted 21 March 2014 - 01:35 AM
Edited by normalizing, 21 March 2014 - 01:38 AM.
Posted 21 March 2014 - 04:53 PM
Edited by OpaqueMind, 21 March 2014 - 04:54 PM.
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