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    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

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Senior Member
Midwest USA
I experimented with hydergine last fall (OK, OK, I took it twice, LOL) but it wasn't a miracle for me. I read about it's effects in Dr Goldstein's book and it looked like a reasonable thing to try.

Now I'm curious if maybe this related drug, nicergoline, is a better fit for MECFS than hydergine anyway.

Since some POTS patients may have antibodies to the a-1 adrenoceptors, it seems like it might help for that as well in a subgroup.

I'm also interested in the possibility of boosting nerve growth factor, which is how I stumbled upon it. It seems like boosting nerve growth factor can calm down the glial cells too.

Has anyone tried it? It looks to be OTC in some countries, but of course not here in the US.

Nicergoline is involved in a number of processes that contribute to dementia symptom improvement. Nicergoline strongly interacts with a blood vessel constriction related protein called α1-adrenoceptors. Because nicergoline was originally designed to treat a vascular condition, it is not surprising that it blocks activation of the α1-adrenoceptor resulting in:

  • dilation of blood vessels
  • reduced blood flow resistance
  • increased blood flow.
Nicergoline has also been shown to affect neurotransmitters in the brain.

Similar to hydergine, nicergoline modulates levels of catecholaminergic neurotransmitters by enhancing the removal of noradrenaline and dopamine.

The fight-or-flight response in the face of a threat or challenge also elicits dopamine and noradrenaline release.

Nicergoline also influences levels of another neurotransmitter, acetylcholine, in the hippocampus. This ia a region of the brain vital to learning and memory. As expected, treatment with nicergoline likely improves memory.

Nicergoline activates major signaling pathways. Moreover, it's thought to influence neuronal activity and the synthesis of proteins that contribute to dementia related diseases.

It also stimulates release of nerve growth factor (NGF). NGF

  • promotes nerve tissue growth
  • protects neurons from degradation
  • prevents the loss of cholinergic neurons
Lastly, nicergoline stimulates increased use of oxygen and glucose, a sugar that provides the body with energy, among the neuron cells.

Treatment with nicergoline has both short and long term effects. In the short term, nicergoline improves cognition and behavior in as little as two months. However, the longer treatments have a greater impact on dementia symptom reduction.

There are some drawbacks to nicergoline use. Patients who respond best to nicergoline tend to be younger with less severe symptoms than patients with low or no response.

Like hydergine, some studies found that patients with vascular dementia experienced more beneficial effects than patients with other types of dementia. However, other studies have not detected a difference in the effectiveness in patients with different forms of dementia.


Senior Member
Midwest USA
We examined the neuroprotective role of nicergoline in neuron –microglia or neuron–astrocytes co-cultures. Nicergoline, an ergoline derivative, significantly suppressed the neuronal cell death induced by co-culture with activated microglia or astrocytes stimulated with lipopolysaccharide (LPS) and interferon (IFN)-g.

To elucidate the mechanism by which nicergoline exerts a neuroprotective effect, we examined the production of inflammatory mediators and neurotrophic factors in activated microglia and astrocytes following nicergoline

In microglia stimulated with LPS and IFN-g, nicergoline suppressed the production of superoxide anions, interleukin (IL)-1h, IL-6, and tumor necrosis factor (TNF)-a in a dose-dependent manner.

In astrocytes, nicergoline also suppressed the production of proinflammatory cytokines and enhanced brain-derived neurotrophic factor (BDNF).

Thus, nicergoline-mediated neuroprotection resulted primarily from the inhibition of inflammatory mediators and the upregulation of neurotrophic factors by glial cells.

Protective effects of nicergoline against neuronal cell death induced by activated microglia and astrocytes (PDF Download Available).

Available from: https://www.researchgate.net/public...induced_by_activated_microglia_and_astrocytes