Modulation of hippocampal ACh release by chronic nicergoline treatment in freely moving young and aged rats

Carfagna, Nicola; Clemente, Angelo Di; Cavanus, S.; Damiani, Domenico; Gerna, M.; Salmoiraghi, P.; Cattaneo, Barbara; Post, Claes

doi:10.1016/0304-3940(95)11928-p

Cited by 31 publications

(9 citation statements)

References 21 publications

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“…As an alpha α1‐adrenoceptor antagonist, nicergoline may have caused vasodilation, which in turn improved cerebral circulation . Nicergoline has been shown to stimulate cholinergic neurotransmission, a system that has been attributed to the pathology of AD, both by increasing acetylcholine release from cholinergic nerve terminals and by inhibiting its degradation . Moreover, nicergoline may exert a positive effect on the neuronal signal transduction system by stimulating the phosphoinositide pathway, which has been reported to be impaired in AD .…”

Section: Discussionmentioning

confidence: 99%

Effects of nicergoline treatment on regional cerebral blood flow in early Alzheimer's disease

Jeong

et al. 2019

Int J Imaging Syst Tech

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Alzheimer's disease (AD) is associated with reduction of regional cerebral blood flow (rCBF) in various brain regions. Although nicergoline has been used to treat cognitive impairment in various types of dementia, the effect of nicergoline on brain perfusion in AD has not been elucidated. The aim of the study was to examine the effect of nicergoline on rCBF in patients with early AD using technetium‐99m hexamethylpropylene amine oxime single‐photon emission computed tomography (SPECT). For 1.7 years on average, 22 patients with early AD received nicergoline (30 mg twice daily) and acetylcholinesterase inhibitors (AChEI), whereas other 22 patients received AChEI only. All patients underwent assessment of dementia severity and SPECT scans at baseline and follow‐up. We compared baseline rCBF and annual percent change of rCBF between the two groups. There were no significant differences in rCBF between the groups at baseline. Although changes in dementia severity was not statistically different, the annual percent changes of rCBF were higher in the left temporal pole (−0.12 ± 3.95 vs −3.38 ± 3.30, P = 0.002) and middle cingulate gyrus (1.91 ± 3.58 vs −1.34 ± 3.17, P = 0.002) among the nicergoline group. Our study demonstrated that nicergoline treatment combined with AChEI either better preserves or further improves cerebral perfusion in the temporal and cingulate cortices in patients with early AD compared to AChEI treatment alone. These results may indicate potential beneficial effects of nicergoline on brain functions in AD.

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Section: Discussionmentioning

confidence: 99%

Effects of nicergoline treatment on regional cerebral blood flow in early Alzheimer's disease

Jeong

et al. 2019

Int J Imaging Syst Tech

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“…15) Nicergoline, a derivative of ergot alkaloid, is an ameliorator of cerebral circulation and metabolism. [16][17][18][19][20][21][22][23][24] In addition to enhancement of cholinergic [25][26][27][28] and dopaminergic transmissions in the brain, 29) protective actions of nicergoline against anoxic and/or ischemic brain damage and neuronal cell death are reported in several cerebral ischemic animals. [18][19][20]30) A recent study showed the neuroprotective action and the reduction of [Glu] o by nicergoline in ischemic rat brains.…”

Section: Glutamate Transporters Limit the Extracellular Concentrationmentioning

confidence: 99%

Nicergoline Enhances Glutamate Uptake via Glutamate Transporters in Rat Cortical Synaptosomes

Nishida

Iwata²,

Kudo

et al. 2004

Biological & Pharmaceutical Bulletin

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To elucidate the mechanisms of neuroprotective action of nicergoline, we examined its effect on glutamate transport in rat cortical synaptosomes and cloned glutamate transporters. In synaptosomes, nicergoline enhanced the glutamate uptake at 1-10 m mM in standard medium and suppressed the increase of extracellular glutamate by reversed transport in low Na ؉ medium. Apparent increase of extracellular glutamate concentration by dihydrokinate, an inhibitor of glial glutamate transporter GLT-1, was antagonized by nicergoline. In Xenopus oocytes expressing mouse neuronal glutamate transporter (mEAAC1), the glutamate-induced inward current was enhanced by nicergoline. These results suggest that nicergoline reduces the extracellular glutamate concentration through its effect on glutamate transporters.

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“…Nicergoline has been demonstrated to increase the availability of acetylcholine through an increased release from cholinergic terminals and a selective inhibition of acetyl cholinesterase 2. Nicergoline may also enhance norepinephrine and dopamine turnover in some areas of the brain 3.…”

Section: Introductionmentioning

confidence: 99%

A systematic review and meta-analysis assessing adverse event profile and tolerability of nicergoline

Fioravanti¹,

Nakashima²,

Xu³

et al. 2014

BMJ Open

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ObjectiveTo evaluate the safety profile of nicergoline compared with placebo and other active agents from published randomised controlled trials.DesignSystematic review and meta-analysis of nicergoline compared with placebo and other active agents across various indications.Data sourcesMEDLINE, Medline-in-process, Cochrane, EMBASE, EMBASE alerts, Cochrane Central Register of Controlled Trials (CENTRAL), Cochrane Database of Systematic Reviews (CDSR) and Cochrane Methodology Register (CMR) for all the randomised controlled trials, open-label or blinded, in adults treated with nicergoline. Studies published until August 2013 were included.Review method29 studies were included for data extraction. The studies included in this review were majorly from European countries and mostly in cerebrovascular disease (n=15) and dementia (n=8).ResultsThe treatment withdrawals were comparatively lower in the nicergoline group as compared with the placebo group (RR=0.92; 95% CI 0.7 to 1.21) and other active comparators (RR=0.45; 95% CI 0.10 to 1.95), but the difference was non-significant. Incidence of any adverse events (AEs) was slightly higher (RR=1.05; 95% CI 0.93 to 1.2) while incidence of serious AEs was lower (RR=0.85; 95% CI 0.50 to 1.45) in the nicergoline compared with placebo group. Frequency of anxiety was significantly lower in nicergoline as compared with placebo (p=0.01). Other AEs including diarrhoea, gastric upset, dizziness and drowsiness were less frequent in the nicergoline group when compared with placebo/active drugs, but the difference was non-significant. Frequency of hypotension and hot flushes was slightly higher in the nicergoline group but the difference was non-significant. None of the studies reported any incidence of fibrosis or ergotism with nicergoline treatment.ConclusionsNicergoline is an ergot derivative, but its safety profile is better than other ergot derivatives like ergotamine and ergotoxine. This systematic review and meta-analysis suggests that nicergoline has a good safety profile. None of the studies included in this systematic review reported any incidence of fibrosis or ergotism with nicergoline.

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Modulation of hippocampal ACh release by chronic nicergoline treatment in freely moving young and aged rats

Cited by 31 publications

References 21 publications

Effects of nicergoline treatment on regional cerebral blood flow in early Alzheimer's disease

Effects of nicergoline treatment on regional cerebral blood flow in early Alzheimer's disease

Nicergoline Enhances Glutamate Uptake via Glutamate Transporters in Rat Cortical Synaptosomes

A systematic review and meta-analysis assessing adverse event profile and tolerability of nicergoline

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