Does generalized hypo-oxygenation (hypoxia) allow endotoxin into the brain through the blood brain barrier, thus increasing the risk for Parkinson disease?

Lange, J. H.; Niehaus, Ines; Cegolon﻿﻿, Luca

doi:10.3325/cmj.2016.57.406

Cited by 3 publications

(4 citation statements)

References 18 publications

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“…However, given that chronic ischemia and hypoxia occur in neurodegenerative diseases, in addition to the OXPHOS, other pathways that participate in HPC include those involved in Parkinson's disease, Huntington's disease, Alzheimer's disease, and pathways of antigen processing and presentation (34)(35)(36). Topological analysis of the network revealed that 14-3-3β (Ywhab), which is related both to cPKCβII and OXPHOS as another candidate molecule involved in HPC (33).…”

Section: Pathway Analysis Is An Integrated Methodsmentioning

confidence: 99%

cPKC beta II is significant to hypoxic preconditioning in mice cerebrum

Lin

et al. 2020

Front Biosci

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Section: Pathway Analysis Is An Integrated Methodsmentioning

confidence: 99%

cPKC beta II is significant to hypoxic preconditioning in mice cerebrum

Lin

et al. 2020

Front Biosci

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“…Evaluation of Mn exposed workers with those not exposed support these findings in that Mn appears to result in pre-synaptic damage and loss of dopamine responsiveness [1]. However, with the suggestion that damage to the BBB may also be impacting susceptibility to PD these events may only be secondary to the primary insult allowing entry of neurotoxins [8]. Alternatively, Mn has been shown to affect GABAergic neurons.…”

mentioning

confidence: 98%

“…Epidemiological studies have shown a relationship with long-term inhalation of Mn and PD [7]. Investigations [6,8] have suggested that Mn is not the only proposed metal or substance (e.g., other metals, endotoxin) responsible for causation of PD, particularity as related to long-term occupational exposure. Various sections of the brain (e.g., substantia nigra, globus pallidus, putamen, and thalamus) appear to also be affected by this and other metals/substances [6].…”

mentioning

confidence: 99%

“…It is possible, there may be a synergistic or co-impaction relationship with several substances in causation of harm by Mn including occurrence of PD. It is possible that combined interactions may be contributing to various disease states as has been suggested with a leaky blood brain barrier (BBB) and endotoxin [8]. Variations of susceptibility have been suggested regarding Mn and PD [5,9].…”

mentioning

confidence: 99%

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Neurotoxicity of Manganism: An Emerging Issue

Jh¹,

Av²

2017

J Headache Pain Manag

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Hypoxia-Induced Signaling Activation in Neurodegenerative Diseases: Targets for New Therapeutic Strategies

Jha

Sharma

et al. 2018

JAD

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For the maintenance of cellular homeostasis and energy metabolism, an uninterrupted supply of oxygen (O2) is routinely required in the brain. However, under the impaired level of O2 (hypoxia) or reduced blood flow (ischemia), the tissues are not sufficiently oxygenated, which triggers disruption of cellular homeostasis in the brain. Hypoxia is known to have a notable effect on controlling the expression of proteins involved in a broad range of biological processes varying from energy metabolism, erythropoiesis, angiogenesis, neurogenesis to mitochondrial trafficking and autophagy, thus facilitating neuronal cells to endure in deprived O2. On the contrary, hypoxia to the brain is a major source of morbidity and mortality in humans culminating in cognitive impairment, gradual muscle weakness, loss of motor activity, speech deficit, and paralysis as well as other pathological consequences. Further, hypoxia resulting in reduced O2 deliveries to brain tissues is supposed to cause neurodegeneration in both in vivo and in vitro models. Similarly, chronic exposure to hypoxia has also been reportedly involved in defective vessel formation. Such vascular abnormalities lead to altered blood flow, reduced nutrient delivery, and entry of otherwise restricted infiltrates, thereby limiting O2 availability to the brain and causing neurological disabilities. Moreover, the precise mechanistic role played by hypoxia in mediating key processes of the brain and alternatively, in triggering pathological signals associated with neurodegeneration remains mysterious. Therefore, this review elucidates the intricate role played by hypoxia in modulating crucial processes of the brain and their severity in neuronal damage. Additionally, the involvement of numerous pharmacological approaches to compensate hypoxia-induced neuronal damage has also been addressed, which may be considered as a potential therapeutic approach in hypoxia-mediated neurodegeneration.

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Does generalized hypo-oxygenation (hypoxia) allow endotoxin into the brain through the blood brain barrier, thus increasing the risk for Parkinson disease?

Cited by 3 publications

References 18 publications

cPKC beta II is significant to hypoxic preconditioning in mice cerebrum

cPKC beta II is significant to hypoxic preconditioning in mice cerebrum

Neurotoxicity of Manganism: An Emerging Issue

Hypoxia-Induced Signaling Activation in Neurodegenerative Diseases: Targets for New Therapeutic Strategies

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