Iron toxicity, ferroptosis and microbiota in Parkinson’s disease: Implications for novel targets

Carvalho, Fernanda Vidal; Landis, Harold E.; Getachew, Bruk; Diogenes Amaral Silva, Victor; Ribeiro, Paulo R.; Aschner, Michael; Tizabi, Yousef

doi:10.1016/bs.ant.2024.02.001

Cited by 6 publications

(3 citation statements)

References 131 publications

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“…If microglia are overwhelmed, such as during a pathological state, their phenotype changes, and this helps the spread of α-Syn, causing disease progression [ 66 , 85 , 86 ]. In neurodegenerative diseases, microglial activation involves cellular metabolism dysregulation and mitochondrial damage, leading to the accumulation of reactive oxygen species (ROS), amino acids, iron, ferroptosis, and eventual inflammation and cell death [ 66 , 85 , 86 , 87 ]. Recently, it was revealed that circadian rhythm also plays a critical role in microglia activation and function and that the disruption of this rhythm can lead to neurodegenerative diseases [ 88 ].…”

Section: Microglia Synucleinopathiesmentioning

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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Section: Microglia Synucleinopathiesmentioning

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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show abstract

“…If microglia get overwhelmed, such as during a pathological state, their phenotype changes, and this helps the spread of α-Syn causing disease progression [66,85,86]. In neurodegenerative diseases, microglial activation involves cellular metabolism dysregulation and mitochondrial damage, leading to accumulation of reactive oxygen species (ROS), amino acids, iron, ferroptosis and eventual inflammation and cell death [66,[85][86][87]. Recently, it was revealed that the circadian rhythm also plays a critical role in microglia activation and function and that disruption of this rhythm can lead to neurodegenerative diseases [88].…”

Section: Microglia-synucleinopathiesmentioning

confidence: 99%

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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“…The mechanism of ferroptosis indicates its critical role in the development of a broad spectrum of diseases, encompassing neurodegenerative, cardiovascular, metabolic, autoimmune, and hematologic disorders ( Carvalho et al, 2024 ; and see below). Its involvement in ischemia/reperfusion injury and its capacity to suppress tumor growth by inhibiting cell proliferation makes it a promising target for new therapeutic strategies ( Jiang et al, 2021 ).…”

Section: Ferroptosismentioning

confidence: 99%

Ferroptosis as an emerging target in sickle cell disease

Fortuna,

Lima,

Oliveira

et al. 2024

Current Research in Toxicology

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Iron toxicity, ferroptosis and microbiota in Parkinson’s disease: Implications for novel targets

Cited by 6 publications

References 131 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

Ferroptosis as an emerging target in sickle cell disease

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