I've been trialing some things lately.
Today I dosed:
Rasagaline 0.25mg
Rivastigmine 1.25mg (will do this 3 times per day)
Gingko 50mg
Diet Coke 0.5ml
This improved my cognitive dysfunction, anhedonia, emotional range slightly. Bad effects were increased saliva production and nausea /stomach issues from the rivastigmine. I don't know if I will stay on this regime as the benefits are not that big.
I've been thinking of adding PEA to the rasagaline to increase phasic dopamine for anhedonia..
Head pressure is unchanged. It feels like something is inhibiting all of this. Maybe GABA-a potentiation from high Allopregnanolone must be solved before these things have any more potent effect. Long term im looking into restoring GABA/Glutamate balance with GAMSA + LTP agents but I have no further ideas on that yet. https://www.frontiersin.org/articles/10 ... 00132/full
GABAergic neurotransmission is altered in hyperammonemic rats, which show increased GABAergic tone in the cerebellum. Chronic treatment with bicuculline, a GABAA receptor antagonist, restores GABAergic tone, the function of the glutamate-nitric oxide-cGMP pathway in the cerebellum and learning of a discrimination task modulated by this pathway (Cauli et al., 2009). The same effects are induced by treatment with pregnenolone sulfate, a negative allosteric modulator of the GABAA receptor, which also improves motor incoordination caused by increased extracellular GABA in the cerebellum (González-Usano et al., 2013).
Reducing GABAergic tone by treating rats with GR3027, which antagonizes the enhancement of GABAA receptor activation by neurosteroids, also restores spatial memory modulated mainly in the hippocampus (Johansson et al., 2015).
These reports show that reducing either GABAergic tone or neuroinflammation in the hippocampus of hyperammonemic rats improve spatial learning. This suggests that there would be a cross-talk between GABAergic tone and neuroinflammation in the modulation of the mechanisms involved in spatial learning and maybe also in other functions modulated in the hippocampus such as short-term memory or anxiety.