Molecular Insights Into Memory-Enhancing Metabolites of Nicotine in Brain: A Systematic Review

Majdi, Alireza; Kamari, Farzin; Sadigh-Eteghad, Saeed; Gjedde, Albert

doi:10.3389/fnins.2018.01002

Cited by 24 publications

(16 citation statements)

References 99 publications

(123 reference statements)

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“…Therefore, it is hypothesized that the stimulation of nAChRs by nicotine or its analogs activates the PI3K/Akt signaling pathway, which, in turn, regulates learning and memory processes (42,45). Indeed, acute and chronic administration of nicotine was reported to improve cognitive impairment in patients with AD (46)(47)(48). Moreover, acute nicotine administration during electroencephalography (EEG) performed in patients with ad who received cholinesterase inhibitors was found to shift the EEG readings towards normal levels (49).…”

Section: Benefits Of Nicotine In Alzheimer's Disease (Ad)mentioning

confidence: 99%

Molecular insights into the benefits of nicotine on memory and cognition (Review)

Alhowail

2021

Mol Med Rep

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The health risks of nicotine are well known, but there is some evidence of its beneficial effects on cognitive function. The present review focused on the reported benefits of nicotine in the brain and summarizes the associated underlying mechanisms. Nicotine administration can improve cognitive impairment in alzheimer's disease (ad), and dyskinesia and memory impairment in Parkinson's disease (PD). In terms of its mechanism of action, nicotine slows the progression of PD by inhibiting Sirtuin 6, a stress-responsive protein deacetylase, thereby decreasing neuronal apoptosis and improving neuronal survival. In AD, nicotine improves cognitive impairment by enhancing protein kinase B (also referred to as Akt) activity and stimulating phosphoinositide 3-kinase/Akt signaling, which regulates learning and memory processes. Nicotine may also activate thyroid receptor signaling pathways to improve memory impairment caused by hypothyroidism. In healthy individuals, nicotine improves memory impairment caused by sleep deprivation by enhancing the phosphorylation of calmodulin-dependent protein kinase II, an essential regulator of cell proliferation and synaptic plasticity. Furthermore, nicotine may improve memory function through its effect on chromatin modification via the inhibition of histone deacetylases, which causes transcriptional changes in memory-related genes. Finally, nicotine administration has been demonstrated to rescue long-term potentiation in individuals with sleep deprivation, ad, chronic stress and hypothyroidism, primarily by desensitizing α 7 nicotinic acetylcholine receptors. To conclude, nicotine has several cognitive benefits in healthy individuals, as well as in those with cognitive dysfunction associated with various diseases. However, further research is required to shed light on the effect of acute and chronic nicotine treatment on memory function. Contents 1. Introduction 2. Benefits of nicotine in Alzheimer's disease (AD) 3. Benefits of nicotine in Parkinson's disease (PD) 4. Benefits of nicotine on memory processes in patients with thyroid disease 5. Effects of nicotine on cognitive function in healthy individuals 6. Nicotine-induced chromatin modifications may improve memory and learning 7. Electrophysiological effects of nicotine: Strengthening synapses 8. Conclusions

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Section: Benefits Of Nicotine In Alzheimer's Disease (Ad)mentioning

confidence: 99%

Molecular insights into the benefits of nicotine on memory and cognition (Review)

Alhowail

2021

Mol Med Rep

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“…Clinically apply nicotine as a treatment of learning and memory impairment and its underlying disorders, biologically active metabolite is more than just a biomarker of nicotine consumption and has potentially therapeutic value in the treatment of learning and memory declines. 13 The percentage of tooth loss by age group in Monmata village of Kecamatan Lhoong ( Table 2) showed that tooth loss in the smokers group occurred in the age range 56-65 years old where age was included in the elderly so that factors can affect tooth loss. The more increase the age, the greater the periodontal tissue damage that occurs when treatment is not conduct.…”

Section: Discussionmentioning

confidence: 99%

Number of tooth loss in smokers and non-smokers in Monmata Lhoong Village, Aceh Besar District, Indonesia

et al. 2019

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Introduction:Tooth loss is a condition that occurs in most of the world's population. The most common causes of tooth loss are caries and periodontal disease. Periodontal disease can usually increase or getting worse by bad habits such as smoking. Smoking accelerates the course of periodontal disease and decreases salivary secretion, whereby increased the risk of caries incidence. Some components of the cigarette's smoke that can accelerate the course of periodontal diseases are nicotine and tar. The purpose of this study was to determine the difference in the number of tooth loss in smokers and nonsmokers. Methods: This study was a cross-sectional study. The sampling method was by the tables of Isaac and Michael, involving 78 smokers and 78 non-smokers in the village of Monmata Lhoong District. Results: Analysis was performed using the Mann-Whitney test. The result showed a significant difference between tooth loss in smokers and non-smokers (p < 0.05). Conclusion: There is a significant difference between the number of tooth loss in smokers compared to the number of tooth loss in non-smokers. The mean value of smokers is higher than the mean value of non smokers.

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“…Numerous studies in this area have shown that these pathways promote neuronal survival, proliferation, and neurite growth as well as neurotransmitter release in the brain and other tissues ( Eneroth et al, 1977 ; Fuxe et al, 1979 ; Aizenman et al, 1991 ; Sastry, 1995 ; Parain et al, 2001 ; Buccafusco and Terry, 2003 ; Koh et al, 2003 ; de Aguiar et al, 2013 ; Gao et al, 2014 ; Tiwari et al, 2015 ; Majdi et al, 2018 ).…”

Section: The Nicotinic Receptors and Neuronal Survival In The Pd Brainmentioning

confidence: 99%

“…Despite their structural similarities, nicotine, and cotinine, differ in their mechanism of action, properties, behavioral effects, and toxicity profile (nicotine is one hundred times more toxic than cotinine) ( Buccafusco and Terry, 2003 ; Grizzell and Echeverria, 2015 ; Majdi et al, 2018 ). The last decade of research has shown that cotinine has unique pharmacokinetic and pharmacodynamic properties, acting as a very weak nAChR agonist but a positive modulator of the α7nAChRs ( Moran, 2012 ; Grizzell et al, 2014 ; Sadigh-Eteghad et al, 2020 ).…”

Section: Effect Of Cotinine Preventing Amyloid-β Peptides Accumulation and Promoting Synaptic Plasticity In The Brainmentioning

confidence: 99%

Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson’s Disease

2021

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Parkinson’s disease (PD) is a neurodegenerative condition characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) in the midbrain resulting in progressive impairment in cognitive and motor abilities. The physiological and molecular mechanisms triggering dopaminergic neuronal loss are not entirely defined. PD occurrence is associated with various genetic and environmental factors causing inflammation and mitochondrial dysfunction in the brain, leading to oxidative stress, proteinopathy, and reduced viability of dopaminergic neurons. Oxidative stress affects the conformation and function of ions, proteins, and lipids, provoking mitochondrial DNA (mtDNA) mutation and dysfunction. The disruption of protein homeostasis induces the aggregation of alpha-synuclein (α-SYN) and parkin and a deficit in proteasome degradation. Also, oxidative stress affects dopamine release by activating ATP-sensitive potassium channels. The cholinergic system is essential in modulating the striatal cells regulating cognitive and motor functions. Several muscarinic acetylcholine receptors (mAChR) and nicotinic acetylcholine receptors (nAChRs) are expressed in the striatum. The nAChRs signaling reduces neuroinflammation and facilitates neuronal survival, neurotransmitter release, and synaptic plasticity. Since there is a deficit in the nAChRs in PD, inhibiting nAChRs loss in the striatum may help prevent dopaminergic neurons loss in the striatum and its pathological consequences. The nAChRs can also stimulate other brain cells supporting cognitive and motor functions. This review discusses the cholinergic system as a therapeutic target of cotinine to prevent cognitive symptoms and transition to dementia in PD.

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Molecular Insights Into Memory-Enhancing Metabolites of Nicotine in Brain: A Systematic Review

Cited by 24 publications

References 99 publications

Molecular insights into the benefits of nicotine on memory and cognition (Review)

Molecular insights into the benefits of nicotine on memory and cognition (Review)

Number of tooth loss in smokers and non-smokers in Monmata Lhoong Village, Aceh Besar District, Indonesia

Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson’s Disease

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