Mitochondria in the context of Parkinson's disease

Villacé, Patricia; Mella, Rosa M.; Kortázar, Danel

doi:10.4103/1673-5374.200802

Cited by 12 publications

(4 citation statements)

References 12 publications

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“…Neuroinflammation may also drive oxidative stress through microglial activation and release of NO, with iNOS the enzyme essential for its production increased. NO can cause neuronal mitochondrial dysfunction ( Chitnis and Weiner, 2017 ; Qin et al., 2013 ) and mitochondrial defects lead to impaired energy metabolism and excessive production of ROS, which is problematic especially for dopaminergic neurons due to their high energy demands and reduced antioxidant capacity ( Park et al., 2018 ; Villacé et al., 2017 ). Stereotaxic administration of LPS reduces the activity of mitochondrial complex I of the electron transport chain (ETC) in both the SN and striatum, consistent with reports on reduced activity of mitochondrial complex I in the SN of PD patients ( Choi et al., 2009 ; Hauser and Hastings, 2013 ; Hunter et al., 2017 ; Reeve et al., 2018 ).…”

Section: Lps Models Of Pd: An Overviewmentioning

confidence: 99%

“…Activated microglia facilitate the activation of astrocytes which augment the inflammatory response through additional production of inflammatory cytokines, and reactive oxygen and nitrogen species. Excessive production of these neurotoxic molecules could impair mitochondrial function, resulting in impaired energy metabolism and additional production of reactive oxygen species (ROS), and can reduce antioxidants such as glutathione peroxidase and superoxide dismutase in the brain ( Hauser and Hastings, 2013 ; Park et al., 2018 ; Villacé et al., 2017 ). Stereotaxic LPS also increases iron levels in the substantia nigra (SN), which could catalyse the Fenton reaction of superoxide (O 2 -) and hydrogen peroxide (H 2 O 2 ) to yield hydroxyl radicals (OH − ) which are toxic to the neurons ( Hauser and Hastings, 2013 ).…”

Section: Lps Models Of Pd: An Overviewmentioning

confidence: 99%

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Lipopolysaccharide animal models of Parkinson’s disease: Recent progress and relevance to clinical disease

Deng

Corrigan

Zhai

et al. 2020

Brain, Behavior, & Immunity - Health

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Parkinson’s disease (PD) is one of the most common neurodegenerative movement disorders which is characterised neuropathologically by progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the presence of Lewy bodies (made predominately of α-synuclein) in the surviving neurons. Animal models of PD have improved our understanding of the disease and have played a critical role in the development of neuroprotective agents. Neuroinflammation has been strongly implicated in the pathogenesis of PD, and recent studies have used lipopolysaccharide (LPS), a component of gram-negative bacteria and a potent activator of microglia cells, to mimic the inflammatory events in clinical PD. Modulating the inflammatory response could ameliorate PD associated complications and thus, it is essential to understand the extent to which LPS models reflect human PD. This review will outline the routes of administration of LPS such as stereotaxic, systemic and intranasal, their ability to recapitulate neuropathological markers of PD, and mechanisms of LPS induced toxicity. We will also discuss the ability of the models to replicate motor symptoms and non-motor symptoms of PD such as gastrointestinal dysfunction, olfactory dysfunction, anxiety, depression and cognitive dysfunction.

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Section: Lps Models Of Pd: An Overviewmentioning

confidence: 99%

Section: Lps Models Of Pd: An Overviewmentioning

confidence: 99%

Lipopolysaccharide animal models of Parkinson’s disease: Recent progress and relevance to clinical disease

Deng

Corrigan

Zhai

et al. 2020

Brain, Behavior, & Immunity - Health

View full text Add to dashboard Cite

show abstract

“…Neurodegenerative disorders, such as Parkinson’s disease and Alzheimer’s disease, are intricately linked to mitochondrial dysfunction within neuronal cells ( 64 – 66 ). Within the realm of neurodegenerative ailments, BAM15 demonstrates its potential as a neuroprotective agent by enhancing mitochondrial respiration and energy generation ( 8 ).…”

Section: Therapeutic Potential Of Bam15 On Specific Disease Contextsmentioning

confidence: 99%

BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases

Xiong,

Zhang,

et al. 2023

Front. Endocrinol.

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Subcellular organelles dysfunction is implicated in various diseases, including metabolic diseases, neurodegenerative diseases, cancer, and cardiovascular diseases. BAM15, a selective mitochondrial uncoupler, has emerged as a promising therapeutic agent due to its ability to enhance mitochondrial respiration and metabolic flexibility. By disrupting the coupling between electron transport and ATP synthesis, BAM15 dissipates the proton gradient, leading to increased mitochondrial respiration and energy expenditure. This review provides a comprehensive overview of BAM15, including its mechanism of action and potential therapeutic applications in diverse disease contexts. BAM15 has shown promise in obesity by increasing energy expenditure and reducing fat accumulation. In diabetes, it improves glycemic control and reverses insulin resistance. Additionally, BAM15 has potential in non-alcoholic fatty liver disease, sepsis, and cardiovascular diseases by mitigating oxidative stress, modulating inflammatory responses, and promoting cardioprotection. The safety profile of BAM15 is encouraging, with minimal adverse effects and remarkable tolerability. However, challenges such as its high lipophilicity and the need for alternative delivery methods need to be addressed. Further research is necessary to fully understand the therapeutic potential of BAM15 and optimize its application in clinical settings.

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“…The increased incidence of aging-associated diseases has initiated intensive research in this field (Prince et al, 2013). In particular, many (Bossy-Wetzel et al, 2008;Fang et al, 2019;Kerr et al, 2017;Villace et al, 2017). Grimm and Eckert found that unhealthy mitochondria are associated with increased levels of reactive oxygen species (ROS) and ATP deficits (Grimm & Eckert, 2017).…”

Section: Introductionmentioning

confidence: 99%

Flavonoids mitigate neurodegeneration in aged Caenorhabditis elegans by mitochondrial uncoupling

Cho

Song

Cho

2020

Food Science & Nutrition

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Mitochondria in the context of Parkinson's disease

Cited by 12 publications

References 12 publications

Lipopolysaccharide animal models of Parkinson’s disease: Recent progress and relevance to clinical disease

Lipopolysaccharide animal models of Parkinson’s disease: Recent progress and relevance to clinical disease

BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases

Flavonoids mitigate neurodegeneration in aged Caenorhabditis elegans by mitochondrial uncoupling

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