Nicotine improved the olfactory impairment in MPTP-induced mouse model of Parkinson's disease

Yang, Jing; Lv, Dong-Jun; Li, Ling-Xi; Wang, Yali; Qi, Di; Chen, Jing; Mao, Cheng‐Jie; Wang, Fen; Liu, Yi; Hu, Lifang; Liu, Chunfeng

doi:10.1016/j.neuro.2019.02.008

Cited by 23 publications

(21 citation statements)

References 28 publications

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“…The ameliorative effect of nicotine on olfactory dysfunction is also shown in the MPTP-induced PD mouse model. Nicotine attenuated the deficit in odor discrimination and detection, the loss of choline acetyltransferase expression in the OB, and the loss of cholinergic neurons and dopaminergic input in the horizontal limb of the diagonal band in MPTP-treated mouse brains (Yang et al 2019 ).…”

Section: Olfactory Dysfunctionmentioning

confidence: 99%

Recent advances in the pathology of prodromal non-motor symptoms olfactory deficit and depression in Parkinson’s disease: clues to early diagnosis and effective treatment

2021

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Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by movement dysfunction due to selective degeneration of dopaminergic neurons in the substantia nigra pars compacta. Non-motor symptoms of PD (e.g., sensory dysfunction, sleep disturbance, constipation, neuropsychiatric symptoms) precede motor symptoms, appear at all stages, and impact the quality of life, but they frequently go unrecognized and remain untreated. Even when identified, traditional dopamine replacement therapies have little effect. We discuss here the pathology of two PD-associated non-motor symptoms: olfactory dysfunction and depression. Olfactory dysfunction is one of the earliest non-motor symptoms in PD and predates the onset of motor symptoms. It is accompanied by early deposition of Lewy pathology and neurotransmitter alterations. Because of the correlation between olfactory dysfunction and an increased risk of progression to PD, olfactory testing can potentially be a specific diagnostic marker of PD in the prodromal stage. Depression is a prevalent PD-associated symptom and is often associated with reduced quality of life. Although the pathophysiology of depression in PD is unclear, studies suggest a causal relationship with abnormal neurotransmission and abnormal adult neurogenesis. Here, we summarize recent progress in the pathology of the non-motor symptoms of PD, aiming to provide better guidance for its effective management.

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Section: Olfactory Dysfunctionmentioning

confidence: 99%

Recent advances in the pathology of prodromal non-motor symptoms olfactory deficit and depression in Parkinson’s disease: clues to early diagnosis and effective treatment

2021

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“…The established anti‐inflammatory effects of nicotine, together with its capability to improve olfactory impairment in a mouse model of Parkinson’s disease [74], provide further credence to its potential usefulness in COVID‐19, as loss of smell is also a common symptom of COVID‐19 [75]. Moreover, nicotine might counter some of the neurological effects of COVID‐19, not only because of its anti‐inflammatory, but also because of its neuroprotectant and mood improvement properties [13–15].…”

Section: Covid‐19—nachrs—cnsmentioning

confidence: 99%

Nicotine and the nicotinic cholinergic system in COVID‐19

et al. 2020

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There is an urgent need to address the devastating pandemic, COVID‐19, caused by SARS‐CoV‐2. The efforts to understand the details of this disease in hope of providing effective treatments are commendable. It is clear now that the virus can cause far more damage in patients with comorbid conditions—particularly in those with respiratory, cardiovascular, or immune‐compromised system—than in patients without such comorbidities. Drug use can further exacerbate the condition. In this regard, the ill effects of smoking are amply documented, and no doubt can be a confounding factor in COVID‐19 progression. Although conflicting hypotheses on the potential role of nicotine in COVID‐19 pathology have recently been offered, we believe that nicotine itself, through its interaction with the nicotinic cholinergic system, as well as ACE2, may not only be of use in a variety of neuropsychiatric and neurodegenerative diseases, but may also be of potential use in COVID‐19. Thus, on one hand, while we strongly support smoking cessation as a means of harm reduction associated with COVID‐19, on the other hand, we support a potential therapeutic role for nicotine, nicotinic agonists, or positive allosteric modulators of nicotinic cholinergic receptors in COVID‐19, owing to their varied effects including mood regulation, anti‐inflammatory, and purported interference with SARS‐CoV‐2 entry and/or replication.

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“…Nicotine at low doses has been reported to have no damaging effects on neuronal populations. However, at high doses, the neurotoxic effects are obvious (Guan et al, 2003;Chambers et al, 2013;Yang et al, 2019). Moreover, previous research indicated that nicotine induces cellular damage both in vitro and in vivo due to the increased lipid peroxidation, creation of reactive oxygen species and oxidative stress (Kalpana et al, 2004;Ayala et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Many in vivo and in vitro studies postulated that nicotine might be neuroprotective for neuronal populations submitted to toxic or ischemic insults (Chambers et al, 2013;Iwamoto et al, 2013;Yang et al, 2019). However, several previous studies have highlighted the brain-damaging properties of nicotine in different cerebral regions (Chen et al, 2003).…”

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confidence: 99%

Effects of Nicotine and Its Withdrawal on The Postnatal Development of Rat Mitral Cells

Amer

Zaghloul

2021

Egyptian Academic Journal of Biological Sciences, D. Histology

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INTRODUCTIONCigarette smoking is considered the most prevalent type of substance dependence, causing serious public health-related problems worldwide. Nicotine is the main chemical substance in cigarettes with cognitive-enhancing effects that make it hard to quit smoking (Valentine and Sofuoglu, 2018; Fowler et al., 2020). Many brain imaging reports have shown activation of the brain centers responsible for attention and working memory performance after nicotine exposure (Rose et al., 2003). Nicotine also acts as an agonist in presynaptic nicotinic acetylcholine receptors, thus facilitating the synaptic release of several neurotransmitters (Singer et al., 2004).

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Nicotine improved the olfactory impairment in MPTP-induced mouse model of Parkinson's disease

Cited by 23 publications

References 28 publications

Recent advances in the pathology of prodromal non-motor symptoms olfactory deficit and depression in Parkinson’s disease: clues to early diagnosis and effective treatment

Recent advances in the pathology of prodromal non-motor symptoms olfactory deficit and depression in Parkinson’s disease: clues to early diagnosis and effective treatment

Nicotine and the nicotinic cholinergic system in COVID‐19

Effects of Nicotine and Its Withdrawal on The Postnatal Development of Rat Mitral Cells

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