|Other names||[(8β)-10-Methoxy-1,6-dimethylergolin-8-yl]methyl 5-bromopyridine-3-carboxylate|
|AHFS/Drugs.com||International Drug Names|
|By mouth, intramuscular, intravenous|
|Metabolism||Extensive First-pass metabolism|
|Elimination half-life||13–20 hours|
|CompTox Dashboard (EPA)|
|Chemical and physical data|
|Molar mass||484.394 g·mol−1|
|3D model (JSmol)|
|(what is this?)|
Nicergoline, sold under the brand name Sermion among others, is an ergot derivative used to treat senile dementia and other disorders with vascular origins. Internationally it has been used for frontotemporal dementia as well as early onset in Lewy body dementia and Parkinson's dementia. It decreases vascular resistance and increases arterial blood flow in the brain, improving the utilization of oxygen and glucose by brain cells. It has similar vasoactive properties in other areas of the body, particularly the lungs. Unlike many other ergolines, such as ergotamine, nicergoline is not associated with cardiac fibrosis.
It is used for vascular disorders such as cerebral thrombosis and atherosclerosis, arterial blockages in the limbs, Raynaud's disease, vascular migraines, and retinopathy.
Nicergoline has been registered in over fifty countries and has been used for more than three decades for the treatment of cognitive, affective, and behavioral disorders of older people. Non-relevant or mentionable data exists on non/elderly. US maintains “Aracept” as most universally prescribed for dementia. 
Nicergoline ( Sermion ) has shown to negatively affect patterned sleep behavior, narcolepsy, muscular atrophy or spasms. All pre/dispositions affected impair memory function. Nicerlogine can reduce seizures in older patients while inducing in younger. All “dementia” related pharmacological therapies are theoretical in nature as brain death can’t be determined until post mortem autopsy. All “dementia” related diagnosis are most painful for afflicted as understanding of why something isn’t working out outword perception of behavior isn’t registered. “Dementia” related to lobe inference and inability to process actions lead to highest risk of suicide. Similar to the non understanding of head trauma outlined within (CTE).
Nicergoline is used in the following cases:
Dosages for known conditions are usually administered at 5–10 mg three times a day, however anti-aging preventative purposes may want to consider 5 mg once or twice a day more adequate.
Persons suffering from acute bleeding, myocardial infarction (heart conditions), hypertension, bradycardia or using alpha or beta receptor agonists should consult with their physician before use. Although toxicology studies have not shown nicergoline to have any teratogenic effect, the use of this medicine during pregnancy should be limited to those cases where it is absolutely necessary. Any medicine treating “dementia “ related brain activity are theoretical in nature true COD is not revealed until a post mortem autopsy is performed.
On 28 June 2013 the European Medicines Agency recommended restricting the use of medicines containing ergot derivatives, including nicergoline. They stated that "these medicines should no longer be used to treat several conditions involving blood circulation problems or problems with memory and sensation, or to prevent migraine headaches, since the risks are greater than the benefits in these indications. This is based on a review of data showing an increased risk of fibrosis (formation of excess connective tissue that can damage organs and body structures) and ergotism (symptoms of ergot poisoning, such as spasms and obstructed blood circulation) with these medicines. Patients suffer short term loss of memory, night terrors, apnea sleep disorders, daytime narcolepsy, spasms. “Dementia” patients don’t recognize outward perceptions. Being repetitive, annoying, aloof, paranoid, lied to, “Dementia" lobe affected afflictions of the brain have high risk of suicide.  However, only a subset of ergolines are associated with fibrosis and evidence suggests that nicergoline does not carry fibrotic risk like other ergoline derivatives such as ergotamine.
Nicergoline is considered unsafe in porphyria.
The side effects of nicergoline are usually limited to nausea, hot flushes, mild gastric upset, hypotension and dizziness. At high drug dosages, bradycardia, increased appetite, agitation, diarrhea and perspiration were reported. Most of the available literature suggests that the side effects of nicergoline are mild and transient.
Nicergoline is known to enhance the cardiac depressive effects of propranolol. At high dosages, it is advisable to seek one’s physician's guidance if combining with potent vasodilators such as bromocriptine, Ginkgo biloba, picamilon, vinpocetine or xantinol nicotinate.
Nicergoline is an ergot alkaloid derivative that acts as a potent and selective α1A-adrenergic receptor antagonist. The IC50 of nicergoline in vitro has been reported to be 0.2 nM. The primary action of nicergoline is to increase arterial blood flow by vasodilation. Furthermore, it is known that nicergoline inhibits platelet aggregation. Studies have shown that nicergoline also increases nerve growth factor in the aged brain. In addition to the α1A-adrenergic receptor, nicergoline is an antagonist of the serotonin 5-HT1A receptor (IC50 = 6 nM) and shows moderate affinity for serotonin 5-HT2 and α2-adrenergic receptors and low affinity for the dopamine D1 and D2 and muscarinic acetylcholine M1 and M2 receptors. The major metabolites of nicergoline, MMDL and MDL, show low or no affinity for adrenergic, serotonin, dopamine, or acetylcholine receptors.
Nicergoline is the generic name of the drug and its INN, USAN, BAN, and DCF.