Butyrate Protects and Synergizes with Nicotine against Iron- and Manganese-induced Toxicities in Cell Culture

Tizabi, Yousef; Getachew, Bruk; Aschner, Michael

doi:10.1007/s12640-023-00682-z

Cited by 4 publications

(4 citation statements)

References 38 publications

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“…Similarly, the damage inflicted by aminochrome, a neurotoxic molecule derived from DA oxidation, on RCSN-3 cells (derived from substantia nigra of adult rat), could also be prevented by nicotine [190]. More recently, protective effects of nicotine against the toxicity induced by manganese and iron in SH-SY5Y cells with implications for PD were reported [187,188]. Additionally, it was shown in-vitro that nicotine protects PC12 neural cells against toxicity induced by1-methyl-4-phenylpyridinium ion (MPP+), via activation of alpha7 nAChR/PI3K/Trx-1 signaling and suppression of endoplasmic reticulum stress [191,192].…”

Section: Nicotine For Pdmentioning

confidence: 98%

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Soares,

Costa,

Ferrolho

et al. 2024

Preprint

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Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, postural instability, that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) is the primary neurotransmitter involved in this disease, but cholinergic imbalance has also been implicated. Current intervention in PD is focused on replenishing central DA, which provides remarkable temporary symptomatic relief but does not address the neuronal loss and the progression of the disease. It has been well established that neuronal nicotinic cholinergic receptors (nAChRs) can regulate DA release and that nicotine itself may have neuroprotective effects. Recent studies have identified nAChRs in nonneuronal cell types including glial cells, where they may regulate inflammatory responses. Given the crucial role of neuroinflammation in dopaminergic degeneration, and the involvement of microglia and astrocytes in this response, glial nAChRs may provide a novel therapeutic target in prevention and/or treatment of PD. In this review, following a brief discussion of PD, we focus on the role of glial cells and specifically their nAChRs in PD pathology and/or treatment.

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Section: Nicotine For Pdmentioning

confidence: 98%

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Soares,

Costa,

Ferrolho

et al. 2024

Preprint

View full text Add to dashboard Cite

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“…Salsolinol, an endogenous product of aldehyde and DA condensation, is frequently used to induce selective toxicity to dopaminergic neurons. SH-SY5Y cells, derived from human neuroblastoma, are commonly used as a cellular model of dopaminergic neurons to investigate novel treatments for PD [ 187 , 188 ]. It is now evident that both alpha4-beta2 and alpha7 nicotinic receptors are involved in the protective effects of nicotine [ 3 , 186 , 189 ].…”

Section: Nicotine For Pdmentioning

confidence: 99%

“…Similarly, the damage inflicted by aminochrome, a neurotoxic molecule derived from DA oxidation, on RCSN-3 cells (derived from substantia nigra of adult rats) could also be prevented by nicotine [ 190 ]. More recently, the protective effects of nicotine against the toxicity induced by manganese and iron in SH-SY5Y cells with implications for PD were reported [ 187 , 188 ]. Additionally, it was shown in vitro that nicotine protects PC12 neural cells against toxicity induced by1-methyl-4-phenylpyridinium ion (MPP+) via activation of alpha7 nAChR/PI3K/Trx-1 signaling and suppression of endoplasmic reticulum stress [ 191 , 192 ].…”

Section: Nicotine For Pdmentioning

confidence: 99%

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Soares,

Costa,

Ferrolho

et al. 2024

Cells

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Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, and postural instability that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) is the primary neurotransmitter involved in this disease, but cholinergic imbalance has also been implicated. Current intervention in PD is focused on replenishing central DA, which provides remarkable temporary symptomatic relief but does not address neuronal loss and the progression of the disease. It has been well established that neuronal nicotinic cholinergic receptors (nAChRs) can regulate DA release and that nicotine itself may have neuroprotective effects. Recent studies identified nAChRs in nonneuronal cell types, including glial cells, where they may regulate inflammatory responses. Given the crucial role of neuroinflammation in dopaminergic degeneration and the involvement of microglia and astrocytes in this response, glial nAChRs may provide a novel therapeutic target in the prevention and/or treatment of PD. In this review, following a brief discussion of PD, we focus on the role of glial cells and, specifically, their nAChRs in PD pathology and/or treatment.

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“…Mn deficiency can lead to weakness, seizures, infertility and bone malformation. Mn overload, on the other hand, concentrates in the brain especially in the basal ganglia resulting in parkinsonism [126]. Early life exposure to high levels of Mn is thought to impact neurodevelopment, especially cognitive behavior in children [127].…”

Section: Manganese (Mn) -Hdmentioning

confidence: 99%

Heavy Metals Interactions with Neuroglia and Gut Microbiota: Implications for Huntington’s Disease

Tizabi,

Bennani,

El Kouhen

et al. 2024

Preprint

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Huntington’s disease (HD) is a rare but progressive and devastating neurodegenerative disease characterized by involuntary movements, cognitive decline, executive dysfunction, and neuropsychiatric conditions such as anxiety and depression. It follows an autosomal dominant inheritance pattern. Thus, a child who has a parent with the mutated huntingtin (mHTT) gene has a 50% chance of developing the disease. Since HTT protein is involved in many critical cellular processes including neurogenesis, brain development, energy metabolism, transcriptional regulation, synaptic activity, vesicle trafficking, cell signaling, and autophagy, its aberrant aggregates lead to disruption of numerous cellular pathways and neurodegeneration. Essential heavy metals are vital at low concentrations, however, at higher concentrations, can exacerbate HD by disrupting the glial-neuronal communication, and/or causing dysbiosis (disturbance in the gut microbiota, GM), both of which can lead to neuroinflammation and further neurodegeneration. Here, we discuss in detail the interactions of iron, manganese and copper with glial-neuron communication and GM and indicate how this knowledge may pave the way for development of a new generation of disease-modifying therapies in HD.

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Butyrate Protects and Synergizes with Nicotine against Iron- and Manganese-induced Toxicities in Cell Culture

Cited by 4 publications

References 38 publications

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

Heavy Metals Interactions with Neuroglia and Gut Microbiota: Implications for Huntington’s Disease

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