The Aging Enteric Nervous System

Nguyen, Tinh Thi; Baumann, Peter; Tüscher, Oliver; Schick, Sandra

doi:10.3390/ijms24119471

Cited by 11 publications

(2 citation statements)

References 133 publications

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“…Similarly, L-tryptophan and L-tyrosine, which is the precursor of L-dopa, were also negatively correlated with age in serum. These metabolites are involved in the synthesis and catabolism of multiple neurotransmitters [79,80], and have potential links to age-related neuropsychiatric disorders [81,82]. Our findings provided further support for earlier studies that microbiota-metabolite pathways in the metabolism of multiple neurotransmitters are crucial in regulating aging phenotypes [83,84].…”

Section: Discussionsupporting

confidence: 85%

Multi-Omics Analysis Reveals Age-Related Microbial and Metabolite Alterations in Non-Human Primates

Chen,

Liu,

et al. 2023

Microorganisms

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Aging is a systemic physiological degenerative process, with alterations in gut microbiota and host metabolism. However, due to the interference of multiple confounding factors, aging-associated molecular characteristics have not been elucidated completely. Therefore, based on 16S ribosomal RNA (rRNA) gene sequencing and non-targeted metabolomic detection, our study systematically analyzed the composition and function of the gut microbiome, serum, and fecal metabolome of 36 male rhesus monkeys spanning from 3 to 26 years old, which completely covers juvenile, adult, and old stages. We observed significant correlations between 41 gut genera and age. Moreover, 86 fecal and 49 serum metabolites exhibited significant age-related correlations, primarily categorized into lipids and lipid-like molecules, organic oxygen compounds, organic acids and derivatives, and organoheterocyclic compounds. Further results suggested that aging is associated with significant downregulation of various amino acids constituting proteins, elevation of lipids, particularly saturated fatty acids, and steroids. Additionally, age-dependent changes were observed in multiple immune-regulatory molecules, antioxidant stress metabolites, and neurotransmitters. Notably, multiple age-dependent genera showed strong correlations in these changes. Together, our results provided new evidence for changing characteristics of gut microbes and host metabolism during aging. However, more research is needed in the future to verify our findings.

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Section: Discussionsupporting

confidence: 85%

Multi-Omics Analysis Reveals Age-Related Microbial and Metabolite Alterations in Non-Human Primates

Chen,

Liu,

et al. 2023

Microorganisms

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“…9,10 Oxidative stress may be caused by exposure to toxic substances, pesticides [11][12][13] and radiation, 14 but its major source is endogenous, due to electron leakage from the Electron Transport Chain (ETC) [15][16][17][18] during energy production by oxidative phosphorylation in mitochondria. Cells with high energy consumption such as those in the CNS, 9,10,15,19 the cardiovascular system, [20][21][22][23] the gastrointestinal system, [24][25][26][27][28][29][30][31] the urinary system [32][33][34][35][36][37] and the skin 14,38,39 are most vulnerable to oxidative stress. Mitochondria are both a source and a target of oxidative stress.…”

Section: Oxidative Stressmentioning

confidence: 99%

The Redox Stress Test: A novel technique reveals oxidative stress in Parkinson’s disease

Wright

2024

MRAJ

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A novel Redox Stress Test has been developed to identify symptoms of diseases associated with oxidative stress by observing symptom changes induced by short-term activation of the transcription factor Nrf2, to restore redox homeostasis. The Nrf2 pathway is triggered by a herbal preparation, Broccoli Seed Tea, developed to deliver a therapeutic dose of highly bioavailable sulforaphane, a potent activator of Nrf2. We discuss the rationale behind the tea and describe the methods used to optimise the bioavailability of sulforaphane to match the pharmacodynamics of Nrf2 activation. When consumed by people with Parkinson’s disease, the Redox Stress Test induced powerful and concurrent attenuation of a diverse group of Parkinson’s non-motor symptoms, including fatigue, constipation and urinary urgency. Motor symptoms were strictly unaffected. This observation indicates that oxidative stress may be a common factor contributing to non-motor symptoms involving sites in the CNS and peripheral organs. We tentatively interpret the results in terms of a hypothetical model for Parkinson’s Syndrome which we describe as a multisystem redox disorder with reservoirs of the disease in peripheral organs as well as in the brain. Eliminating the disease in peripheral organs is therefore a prerequisite to stopping disease progression in the brain. According to this model, the redox disorder in the brain provokes progressive neurological damage, which is not recognised as such in the early years. More specific neurological symptoms only come to light many years later, when damage to dopaminergic neurons creates a dopamine deficiency which eventually exceeds the threshold required for normal motor control, generating a new coherent group of neurological symptoms which define movement disorder. Given the apparent ease with which oxidative stress can be quenched in several locations simultaneously, we briefly discuss possible implications for public health, medical research, patients and patient advocacy groups. We note that the Redox Stress Test may have the potential to explore symptoms of other diseases where oxidative stress is believed to play a major role, although this remains subject to validation by further research.

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