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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 5 of 5. This is the beginning of the thread.
Posted by SLS on February 9, 2019, at 13:16:56
Hi.
Linkadge has been interested in Trk-B for a long time. Trk is the abbreviation for tropomyosin receptor kinase. Blocking this receptor is how most current biologics work when treating autoimmune diseases. However, activating this receptor might act to improve depression. One study of rodents found that all of the antidepressants they tested increased Trk-B. The authors suggested that perhaps this a common thread linking the different classes of antidepressants. Apparently, BDNF is not necessary for this effect on Trk-B.
- Scott
Posted by bleauberry on February 10, 2019, at 13:28:38
In reply to Does anyone know how to activate Trk-B?, posted by SLS on February 9, 2019, at 13:16:56
Curcumin has influence. Some mention of Niacin.
> Hi.
>
> Linkadge has been interested in Trk-B for a long time. Trk is the abbreviation for tropomyosin receptor kinase. Blocking this receptor is how most current biologics work when treating autoimmune diseases. However, activating this receptor might act to improve depression. One study of rodents found that all of the antidepressants they tested increased Trk-B. The authors suggested that perhaps this a common thread linking the different classes of antidepressants. Apparently, BDNF is not necessary for this effect on Trk-B.
>
>
> - Scott
Posted by bleauberry on February 10, 2019, at 13:30:32
In reply to Does anyone know how to activate Trk-B?, posted by SLS on February 9, 2019, at 13:16:56
Not sure of meds. Do a search on herb or herbal effects on Trk-B and there are results for that.
> Hi.
>
> Linkadge has been interested in Trk-B for a long time. Trk is the abbreviation for tropomyosin receptor kinase. Blocking this receptor is how most current biologics work when treating autoimmune diseases. However, activating this receptor might act to improve depression. One study of rodents found that all of the antidepressants they tested increased Trk-B. The authors suggested that perhaps this a common thread linking the different classes of antidepressants. Apparently, BDNF is not necessary for this effect on Trk-B.
>
>
> - Scott
Posted by linkadge on February 14, 2019, at 15:19:42
In reply to Does anyone know how to activate Trk-B?, posted by SLS on February 9, 2019, at 13:16:56
In the case of amitriptyline, it directly activates the trk-b receptors (i.e. directly mimicking BDNF). I don't think other antidepressants directly activate trkb (i.e not trkb agonists), but some directly activate the sigma receptors (which I think can interact or synergise with TRK-B receptors). I know imipramine (somehow) activates the pathway without directly binding to trk-b. A combination of fluvoxamine (sigma agonist) and amitriptyline (TRK-B) agonist, could be a synergistic 'neurotrophic' combination.
I'm not sure of the mechanism of how other antidepressants activate TRK-B. It may be related to epigenetics (i.e controlling receptor sensitivity) or perhaps some alternative binding site (sorry, I'm only an armchair biologist).
rTMS activates the BDNF pathways (even outside the brain) suggesting a non-neurotransmitter mechanism for activation.
This flavonoid "7,8-dihydroxyflavone" can be bought as a supplement and supposedly acts as a trkb agonist. GSK3 inhibitors supposedly activate TRKB without BDNF.
Linkadge
Posted by SLS on February 15, 2019, at 16:20:18
In reply to Re: Does anyone know how to activate Trk-B?, posted by linkadge on February 14, 2019, at 15:19:42
Thanks for the information, Linkadge.
One rodent experiment reported that BDNF was not necessary for the activation of Tkr-B. They were surprised.
- Scott
This is the end of the thread.
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