dopamine receptoren vermeerderen?

Chamey schreef:Ik ging twee weken door en plots voelde ik helemaal niets van 140mg.

Zal vast de halfwaardetijd zijn.

Chamey schreef:Dopaminereceptoren vermeerderen?

kan dat? en hoe doe je dat?

JongGeleerd schreef:Dat stimuleert eventueel de release van dopamine, de neurotransmitter. Voor een stimulerende werking op de aanmaak van neuronen (BDNF, Brain Derived Neurotropic Factor) zou ik je focussen op Neurotropics als Noopept.

On the mechanism of noopept action: decrease in activity of stress-induced kinases and increase in expression of neutrophines schreef:The influence of noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111)--a drug combining the nootrope and neuroprotector properties--on the activity of mitogen-activated protein kinases (MAPKs) and the level of NGF and BDNF gene and protein expression in the frontal cortex, hippocampus, and hypothalamus has been studied in rats. Under conditions of chronic administration (28 days, 0.5 mg/day, i.p.), noopept decreased the activity of stress-induced kinases (SAPK/JNK 46/54 and pERK1/2) in rat hippocampus and increases the level of mRNA of the BDNF gene in both hypothalamus and hippocampus. The content of BDNF protein in the hypothalamus was also somewhat increased. In the context of notions about the activation of stress-induced kinases, as an important factor of amyloidogenesis and tau-protein deposition in brain tissue, and the role of deficiency of the neurotrophic factors in the development of neurodegenerative processes, the observed decrease in the activity of stress-activated MAPKs and increased expression of BDNF as a result of noopept administration suggest thatthis drug hasaspecific activity withrespect to some pathogenetic mechanisms involved in the Alzheimer disease.

Noopept stimulates the expression of NGF and BDNF in rat hippocampus. schreef:We studied the effect of original dipeptide preparation Noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111) with nootropic and neuroprotective properties on the expression of mRNA for neurotropic factors NGF and BDNF in rat hippocampus. Expression of NGF and BDNF mRNA in the cerebral cortex and hippocampus was studied by Northern blot analysis. Taking into account the fact that pharmacological activity of Noopept is realized after both acute and chronic treatment, we studied the effect of single and long-term treatment (28 days) with this drug. Expression of the studied neurotropic factors in the cerebral cortex was below the control after single administration of Noopept, while chronic administration caused a slight increase in BDNF expression. In the hippocampus, expression of mRNA for both neurotrophins increased after acute administration of Noopept. Chronic treatment with Noopept was not followed by the development of tolerance, but even potentiated the neurotrophic effect. These changes probably play a role in neuronal restoration. We showed that the nootropic drug increases expression of neurotrophic factors in the hippocampus. Our results are consistent with the hypothesis that neurotrophin synthesis in the hippocampus determines cognitive function, particularly in consolidation and delayed memory retrieval. Published data show that neurotrophic factor deficiency in the hippocampus is observed not only in advanced Alzheimer's disease, but also at the stage of mild cognitive impairment (pre-disease state). In light of this our findings suggest that Noopept holds much promise to prevent the development of Alzheimer's disease in patients with mild cognitive impairment. Moreover, therapeutic effectiveness of Noopept should be evaluated at the initial stage of Alzheimer's disease.

Effect of the novel nootropic and neuroprotective dipeptide noopept on the streptozotocin-induced model of sporadic Alzheimer disease in rats schreef:Streptozotocin-intracerebroventricularly treated rats are proposed as an experimental model of sporadic Alzheimer disease (AD). Diabetogenic toxin streptozotocin (STZ) administered in both cerebral ventricles in a dose of 3 mg/kg decreases the expression of NGF and BDNF mainly in the hippocampus and increases the content of malonic dialdehyde (MDA)--a product of lipid peroxidation--in the brain tissues. These metabolic changes are accompanied by a pronounced cognitive deficiency, which is manifested by long-term memory deterioration in the passive avoidance test. These manifestations of pathology are not accompanied by hyperglycemia in the case of intraventricular STZ administration, in contrast to the systemic (in particular, intraperitoneal) route of introduction that causes a pronounced increase in the blood glucose level. These results are consistent with the existing notions that (i) STZ administered intraventricularly provokes a complex of changes imitating the sporadic AD and (ii) this disease can be considered as a manifestation of type-III diabetes. The new original cognition enhancing and neuroprotective dipeptide noopept decreases the aforementioned metabolic changes and the accompanying long-term deterioration of the memory. Previously, this systemically active dipeptide was shown to be capable of increasing expression of NGF and BDNF in the hippocampus, stimulating the antibody production to beta-amyloid, inhibiting the lipid peroxidation, activating the endogenous antioxidant systems, and decreasing the rate of glutamate release (cholinopositive effect). Taken together, these data indicate that noopept can be considered as a multipotent substance acting upon several important pathogenic chainsof the sporadic AD.

Tuurlijk zullen er onderzoekjes zijn die dan een significante stijging waarnemen op korte termijn oid waar die verkopertjes dan mooie artikelen van maken maar als je na langdurig gebruik stopt met dat soort middelen dan dan zou het mij niks verbazen als een tegengesteld effect ontstaat. Behalve eventuele andere nadelen dan, als de voordelen al stellig bewezen zijn.

Accountz0r schreef:

Tuurlijk zullen er onderzoekjes zijn die dan een significante stijging waarnemen op korte termijn oid waar die verkopertjes dan mooie artikelen van maken maar als je na langdurig gebruik stopt met dat soort middelen dan dan zou het mij niks verbazen als een tegengesteld effect ontstaat. Behalve eventuele andere nadelen dan, als de voordelen al stellig bewezen zijn.

Dit blijft mijn argument.

Uit bovenstaande stukjes kan ik sowieso opmaken dat de hypotheses (volgens mij) te maken hadden met uitstellen of verminderen van de symptomen van Alzheimer.
En sowieso alleen op een specifiek onderdeel in de hormoonhuishouding, niet op de werking van de hersenen als geheel. 28 dagen is sowieso niet echt lang bovendien en ratten zijn ook geen mensen.
Denk dat je ook een onderzoek over suiker zou kunnen maken met soortgelijke resultaten.

Ik ben nog steeds sceptisch. De wetenschappelijke onderbouwing van de gunstige effecten van dit zgn. wondermiddel en anderen die is gewoon te zwak, in mijn ogen.

Accountz0r schreef:MissFappie wil te graag laten zien dat ze wetenschap heeft gedaan geloof ik met al die analyses van modelletjes, geloof ik.