Linking Neuroinflammation and Neurodegeneration in Parkinson’s Disease

Gelders, Géraldine; Baekelandt, Veerle; Perren, Anke Van der

doi:10.1155/2018/4784268

Cited by 368 publications

(290 citation statements)

References 108 publications

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“…Evidence is accumulated to support the involvement of neuroinflammation in neurodegenerative diseases, including Alzheimer's and Parkinson's diseases . TNF‐α is a potent pro‐inflammation cytokine and plays an important role in neuroinflammation .…”

Section: Resultsmentioning

confidence: 99%

“…Evidence is accumulated to support the involvement of neuroinflammation in neurodegenerative diseases, including Alzheimer's and Parkinson's diseases. [51][52][53] TNF-α is a potent pro-inflammation cytokine 13 and plays an important role in neuroinflammation. 47 To determine the effect of repeated TNF-α challenge on learning, cognition, and memory, the spatial learning and memory ability were examined in mice challenged with TNF-α or control vehicle by using the Morris water maze and the novel object recognition (NOR) models.…”

Section: Repeated Tnf-α Challenge Decreased Learning Cognition Andmentioning

confidence: 99%

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Molecular mechanism of tumour necrosis factor alpha regulates hypocretin (orexin) expression, sleep and behaviour

Zhan

Che

Zhao

et al. 2019

J Cellular Molecular Medi

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Hypocretin 1 and hypocretin 2 (orexin A and B) regulate sleep, wakefulness and emotion. Tumour necrosis factor alpha (TNF‐α) is an important neuroinflammation mediator. Here, we examined the effects of TNF‐α treatment on hypocretin expression in vivo and behaviour in mice. TNF‐α decreased hypocretin 1 and hypocretin 2 expression in a dose‐dependent manner in cultured hypothalamic neurons. TNF‐α decreased mRNA stability of prepro‐hypocretin, the single precursor of hypocretin 1 and hypocretin 2. Mice challenged with TNF‐α demonstrated decreased expression of prepro‐hypocretin, hypocretin 1 and hypocretin 2 in hypothalamus. In response to TNF‐α, prepro‐hypocretin mRNA decay was increased in hypothalamus. TNF‐α neutralizing antibody restored the expression of prepro‐hypocretin, hypocretin 1 and hypocretin 2 in vivo in TNF‐α challenged mice, supporting hypocretin system can be impaired by increased TNF‐α through decreasing hypocretin expression. Repeated TNF‐α challenge induced muscle activity during rapid eye movement sleep and sleep fragmentation, but decreased learning, cognition and memory in mice. TNF‐α neutralizing antibody blocked the effects of TNF‐α; in contrast, hypocretin receptor antagonist enhanced the effects of TNF‐α. The data support that TNF‐α is involved in the regulation of hypocretin expression, sleep and cognition. The findings shed some lights on the role of neuroinflammation in neurodegenerative diseases including Alzheimer's disease and Parkinson's disease.

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Section: Resultsmentioning

confidence: 99%

Section: Repeated Tnf-α Challenge Decreased Learning Cognition Andmentioning

confidence: 99%

Molecular mechanism of tumour necrosis factor alpha regulates hypocretin (orexin) expression, sleep and behaviour

Zhan

Che

Zhao

et al. 2019

J Cellular Molecular Medi

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“…Such changes in the offspring's brain may lead to brain dysfunction in the long term. Neuroinflammation has been found in various brain conditions, especially during the development of neurodegenerative disease . Brain aging can also be accelerated by cigarette smoking, which may be replicated in smoker's offspring.…”

Section: Potential Cellular Mechanismsmentioning

confidence: 99%

“…Neuroinflammation has been found in various brain conditions, especially during the development of neurodegenerative disease. 62,63 Brain aging can also be accelerated by cigarette smoking, 64 which may be replicated in smoker's offspring. The formation of β-amyloid, the hallmark of the development of Alzheimer's disease, can be increased if brain levels of TLR4, IL-1, and IL-6 are high.…”

Section: Inflammatory Responses In the Brainmentioning

confidence: 99%

What lessons have we learnt about the impact of maternal cigarette smoking from animal models?

Chan

Oliver

Chen

2019

Clin Exp Pharma Physio

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Maternal first‐ or second‐hand tobacco smoking during pregnancy is still common albeit that the detrimental effects to the unborn child are well known. Maternal tobacco cigarette smoking can affect multiple organ systems in the offspring, rendering them at increased risk of various conditions throughout life (eg. intrauterine underdevelopment, asthma, substance abuse, diabetes). However, this review will only focus on its impact on the brain and the related molecular changes in the offspring based on evidence from animal studies. Although epidemiological studies have identified the associations between maternal cigarette smoke exposure (SE) and brain disorders, animal models can help identify the underlying mechanisms and test interventions. Human studies have found that maternal SE is closely linked to small brain size and changes in brain structure and associated with a high risk of cognitive defects. Animal models suggest that this may be due to increased brain oxidative stress and inflammation during the neonatal period, leading to increased brain cell apoptosis in adulthood. There is a distinct gender bias of such impacts, where male offspring are more affected than females. Female offspring seem to have developed the adaptation by increasing endogenous antioxidant levels. Indeed, animal studies have shown that using antioxidant supplementation during pregnancy can improve neurological outcomes in male offspring, however, the efficacy in humans is yet to be confirmed. Furthermore, some animal studies suggested nicotine as the key player in intrauterine underdevelopment due to maternal SE, while human clinical trials using nicotine replacement therapy do not support this mechanism. This review will discuss the possible reasons.

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“…Interaction network of various pathways involved in pharmacodynamic pathogenesis. The network is generated by referring to recent reviews in the field . Molecular species are shown in green ovals whereas molecular/cellular processes are shown in yellow rectangles.…”

Section: List Of Abbreviationsmentioning

confidence: 99%

Mathematical Biology Models of Parkinson's Disease

Bakshi

Chelliah²,

Chen

et al. 2018

CPT Pharmacom & Syst Pharma

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Parkinsons disease ( PD ) is a progressive neurodegenerative disease with substantial and growing socio‐economic burden. In this multifactorial disease, aging, environmental, and genetic factors contribute to neurodegeneration and dopamine ( DA ) deficiency in the brain. Treatments aimed at DA restoration provide symptomatic relief, however, no disease modifying treatments are available, and PD remains incurable to date. Mathematical modeling can help understand such complex multifactorial neurological diseases. We review mathematical modeling efforts in PD with a focus on mechanistic models of pathogenic processes. We consider models of α‐synuclein (Asyn) aggregation, feedbacks among Asyn, DA , and mitochondria and proteolytic systems, as well as pathology propagation through the brain. We hope that critical understanding of existing literature will pave the way to the development of quantitative systems pharmacology models to aid PD drug discovery and development.

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Linking Neuroinflammation and Neurodegeneration in Parkinson’s Disease

Cited by 368 publications

References 108 publications

Molecular mechanism of tumour necrosis factor alpha regulates hypocretin (orexin) expression, sleep and behaviour

Molecular mechanism of tumour necrosis factor alpha regulates hypocretin (orexin) expression, sleep and behaviour

What lessons have we learnt about the impact of maternal cigarette smoking from animal models?

Mathematical Biology Models of Parkinson's Disease

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