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Need everyone's expertise on BDNF

bdnf 23andme alzheimers cerebrolysin val66met met66met

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#1 Maverick32

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Posted 22 March 2015 - 06:17 PM


 I have received the results of my Promethease and the analysis of my 23andme data.

 

I am the very rare rs6265(A;A) (Met/Met) for the Val66Met polymorphism

 

introversion; depression resistant; impaired motor skills learning Met/met (higher risk) variant of the Val66Met snp in the BDNF gene that codes for brain-derived neurotrophic factor.

Met/met is associated with susceptibility to neuropsychiatric disorders. associated with introversion This genotype may provide resistance to depression when subjected to repeated defeat blog summary On a driving-based motor learning task subjects with this genotype showed greater error during short-term learning and poorer retention over 4 days, relative to subjects without the polymorphism. The presence of this BDNF polymorphism is associated with differences in brain motor system function, altered short-term plasticity, and greater error in short-term motor learning. 

 

Although the val66met polymorphism does not seem to affect the activity of mature BDNF, the intracellular trafficking and activity-dependent secretion of BDNF is altered (Egan et al., 2003). At a cellular level, there appears to be a met-dose effect on intracellular localisation (Chen et al., 2004) and regulation of activity-dependent secretion of BDNF (Chen et al., 2006). Variations in n-acetyl-aspartate (NAA) levels in the hippocampus associated with the met-allele also suggest a functional met-dose effect.

 

Prior to knowing all of this I tried Cerebrolysin for the first time to help with a graduate exam I had previously done poorly on. While on Cerebrolysin I retook the exam and scored significantly higher than my previous score. In fact the range of improvement was considered an outlier according to their past statistics concerning retakes in general. Cerebrolysin improved all aspects of my life. Now I know why.

 

I need everyone's help. I have to find ways to increase BDNF expression. 

1. I am in the US. Obtaining a cerebrolysin prescription seems improbable and so I have ordered online from a vendor. It would just be easier to have a script. Does anyone know how I can obtain one?

2. What supplements should I be taking to increase BDNF? Should I stop Adderall and Memantine? (just began lithium oronate)

 

My father passed away from early-onset Alzheimer's, and my suspicion now is that this and poor lifestyle was the cause. He tested negative for the usual genetic risk factors, APOE4 etc.



#2 Metagene

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Posted 22 March 2015 - 07:43 PM

Semax.

I am rs6265(A;G) APOE3/4
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#3 lostfalco

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Posted 23 March 2015 - 12:35 AM

LLLT might help. 

 

http://www.ncbi.nlm....pubmed/25196192

 

J Biophotonics. 2014 Sep 8;9999(9999). doi: 10.1002/jbio.201400069. [Epub ahead of print]

Low-level laser therapy for traumatic brain injury in mice increases brain derived neurotrophic factor (BDNF) and synaptogenesis.
Abstract

Transcranial low-level laser (light) therapy (LLLT) is a new non-invasive approach to treating a range of brain disorders including traumatic brain injury (TBI). We (and others) have shown that applying near-infrared light to the head of animals that have suffered TBI produces improvement in neurological functioning, lessens the size of the brain lesion, reduces neuroinflammation, and stimulates the formation of new neurons. In the present study we used a controlled cortical impact TBI in mice and treated the mice either once (4 h post-TBI, 1-laser), or three daily applications (3-laser) with 810 nm CW laser 36 J/cm2 at 50 mW/cm2 . Similar to previous studies, the neurological severity score improved in laser-treated mice compared to untreated TBI mice at day 14 and continued to further improve at days 21 and 28 with 3-laser being better than 1-laser. Mice were sacrificed at days 7 and 28 and brains removed for immunofluorescence analysis. Brain-derived neurotrophic factor (BDNF) was significantly upregulated by lasertreatment in the dentate gyrus of the hippocampus (DG) and the subventricular zone (SVZ) but not in the perilesional cortex (lesion) at day 7 but not at day 28. Synapsin-1 (a marker for synaptogenesis, the formation of new connections between existing neurons) was significantly upregulated in lesion and SVZ but not DG, at 28 days but not 7 days. The data suggest that the benefit of LLLT to the brain is partly mediated by stimulation of BDNFproduction, which may in turn encourage synaptogenesis. Moreover the pleiotropic benefits of BDNF in the brain suggest LLLT may have wider applications to neurodegenerative and psychiatric disorders. Neurological Severity Score (NSS) for TBI mice.

© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

 



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#4 kurdishfella

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Posted 27 July 2020 - 09:49 AM

amitrypiline is a potent trka and trkb agonist both which bdnf and ngf bind to . But bdnf and ngf also activate LNGFR which induce cell death. but since amytripyline does not increase bdnf or ngf but just binds to its receptor trka and trkb can this be dangerous because LNGFR Does not get activated together with them and cause tumor or something because too much cells

https://www.ncbi.nlm...les/PMC2844702/

Edited by kurdishfella, 27 July 2020 - 09:50 AM.

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Also tagged with one or more of these keywords: bdnf, 23andme, alzheimers, cerebrolysin, val66met, met66met

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