The Gut-Brain Axis: Two Ways Signaling in Parkinson’s Disease

Dogra, Nitu; Mani, Ruchi Jakhmola; Katare, Deepshikha Pande

doi:10.1007/s10571-021-01066-7

Cited by 55 publications

(42 citation statements)

References 128 publications

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“…Results clearly show that preventive probiotic supplement was able to restore the gut barrier integrity. Several peripheral and central diseases' etiology is also due to deregulation gut microbiota after damage in epithelial barrier function [65,66]. An altered gut microbiota profile is related to metabolic impairment such as obesity [67] and insulin resistance [68] and altered intestinal permeability [69].…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Oral Probiotic Treatment in Paclitaxel-Induced Neuropathic Pain

et al. 2021

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Chemotherapy-induced peripheral neuropathy (CIPN) represents one of the most prevalent and potentially disabling side effects due to the use of anticancer drugs, one of the primary neuropathies detected is peripheral neuropathy induced by administration of taxanes, including paclitaxel. It has been demonstrated that gut microbiota is crucial for the therapeutic effect of chemotherapeutic drugs for inhibiting tumor growth and contributed to the pathogenesis of the CIPN. The use of nutraceuticals has receiving growing attention from the research community due to their phytochemical, biological, and pharmacological properties. It has been demonstrated that probiotic formulations may both reduce inflammation and modulate the expression of pain receptors. Our studies tested the efficacy of a probiotic formulation, SLAB51, in preventing paclitaxel-induced neuropathy. Interestingly, our probiotic formulation was able to keep the gut integrity, preserving its functionality, in CIPN-mice, moreover, it prevented the mechanical and cold hypersensitivity induced in paclitaxel-mice. Additionally, ex-vivo analysis showed that in CIPN-mice the pro-biotic treatment increased the expression of opioid and cannabinoid receptors in spinal cord, it prevented in the reduction in nerve fiber damage in the paws and modulated the serum proinflammatory cytokines concentration. On basis of these data, the use of this specific probiotic formulation may represent a valid adjuvant agent to paclitaxel, useful and not toxic for long-lasting therapies.

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Section: Discussionmentioning

confidence: 99%

Effects of Chronic Oral Probiotic Treatment in Paclitaxel-Induced Neuropathic Pain

et al. 2021

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“…As a bidirectional communication between GI tract and the CNS, the microbiota-gut-brain axis is associated with immune, endocrine mechanisms and neural pathways ( Cryan and O'Mahony, 2011 ; De Palma et al., 2014 ; Sun and Shen, 2018 ; Dogra et al., 2021 ). It modulates the digestion events (such as secretion and motility), immunologic function, and perception or emotional response to visceral stimuli under normal condition ( Mayer et al., 2006 ).…”

Section: The Microbiota-gut-brain Axismentioning

confidence: 99%

Gut Microbiota and Parkinson’s Disease: Implications for Faecal Microbiota Transplantation Therapy

Kang

Zhang

et al. 2021

ASN Neuro

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Parkinson's disease (PD) ranks the second place among neurodegenerative diseases in terms of its morbidity, which affects 1-2% people aged over 65 years. In addition to genetics, some environmental factors may exert vital parts in PD occurrence as well. At present, more and more studies are conducted to elucidate the association between gut microbial dysbiosis and the incidence of PD. Gut microbial dysbiosis has a certain effect on both the central nervous system (CNS) and the enteric nervous system (ENS), which indicates that there is a gut-microbiota-brain axis that induces CNS disorders. Some gut microbial strains are suggested to suppress or weaken the neuroinflammation- and gut-inflammation-immune responses, which suggests the protective and pathogenic effects of certain gut microbial species on PD progression. Therefore, gut microbiome may contain plenty of targets for preventing and managing PD. Faecal microbiota transplantation (FMT) may serve as a direct and useful treatment for PD in the future. Nonetheless, there is little available scientific research in this field. The present work reviewed the latest research to examine the association of gut microbiota with PD, and the future prospects of FMT treatment.

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“…Due to its prion-like protein activation mechanism, α-syn can misfold to cause self-abnormal aggregation, and can also transmit signals amongst nervous cells, and spread throughout the nervous system ( 86 ). Several studies have indicated that the ENS may be the channel by which α-syn is transferred from the PNS to the CNS ( 41 , 87 ).…”

Section: α-Syn Accumulation Contributes To Neurodegeneration In the Cns Of Patients With Pdmentioning

confidence: 99%

“…However, further studies are required to determine the specific mechanisms. In addition, studies have reported that an abnormal GM can enhance the levels of inflammation via the induction of immune responses, leading to the misfolding of α-syn in patients with PD ( 40 , 41 ). The dysfunction of the enteric nervous system (ENS), and the accumulation of anti-α-syn immune response proteins were detected in the ENS ganglia in mice with α-syn mutations (either A53T or A30P from insertions of an entire human SNCA gene) when they were 3 months old ( 42 ).…”

Section: Introductionmentioning

confidence: 99%

Roles of α‑synuclein in gastrointestinal microbiome dysbiosis‑related Parkinson's disease progression (Review)

Lei

et al. 2021

Mol Med Rep

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Parkinson's disease (PD) is the second most common neurodegenerative disease amongst the middle-aged and elderly populations. Several studies have confirmed that the microbiota-gut-brain axis (MGBA) serves a key role in the pathogenesis of PD. Changes to the gastrointestinal microbiome (GM) cause misfolding and abnormal aggregation of α-synuclein (α-syn) in the intestine. Abnormal α-syn is not eliminated via physiological mechanisms and is transported into the central nervous system (CNS) via the vagus nerve. The abnormal levels of α-syn aggregate in the substantia nigra pars compacta, not only leading to the formation of eosinophilic Lewis Bodies in the cytoplasm and mitochondrial dysfunction in dopaminergic (DA) neurons, but also leading to the stimulation of an inflammatory response in the microglia. These pathological changes result in an increase in oxidative stress (OS), which triggers nerve cell apoptosis, a characteristic of PD. This increase in OS further oxidizes and intensifies abnormal aggregation of α-syn, eventually forming a positive feedback loop. The present review discusses the abnormal accumulation of α-syn in the intestine caused by the GM changes and the increased levels of α-syn transport to the CNS via the MGBA, resulting in the loss of DA neurons and an increase in the inflammatory response of microglial cells in the brain of patients with PD. In addition, relevant clinical therapeutic strategies for improving the GM and reducing α-syn accumulation to relieve the symptoms and progression of PD are described. Contents 1. Introduction 2. An aberrant GM affects α-syn accumulation in the intestine of patients with PD 3. α-syn accumulation contributes to neurodegeneration in the CNS of patients with PD 4. Novel treatments based on the MGBA and α-syn for PD 5. Conclusion

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The Gut-Brain Axis: Two Ways Signaling in Parkinson’s Disease

Cited by 55 publications

References 128 publications

Effects of Chronic Oral Probiotic Treatment in Paclitaxel-Induced Neuropathic Pain

Effects of Chronic Oral Probiotic Treatment in Paclitaxel-Induced Neuropathic Pain

Gut Microbiota and Parkinson’s Disease: Implications for Faecal Microbiota Transplantation Therapy

Roles of α‑synuclein in gastrointestinal microbiome dysbiosis‑related Parkinson's disease progression (Review)

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