Exposome, Molecular Pathways and One Health: The Invertebrate Caenorhabditis elegans

Mikecz, Anna von

doi:10.3390/ijms23169084

Cited by 5 publications

(4 citation statements)

References 71 publications

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“…It has a short lifespan of ~3 weeks and undergoes rapid generation cycles, allowing for quick observation of the effects of genetic manipulations across multiple generations. In ALS studies, this characteristic enables researchers to assess the progression of neurodegeneration and the inheritance patterns of genetic mutations associated with the disease in a relatively short timeframe (von Mikecz, 2022 ). C. elegans has a transparent anatomical body that can be used to visualize all cell types at developmental stages (Brenner, 1974 ).…”

Section: C Elegans Modelsmentioning

confidence: 99%

Invertebrate genetic models of amyotrophic lateral sclerosis

Zhou,

2024

Front. Mol. Neurosci.

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Amyotrophic lateral sclerosis (ALS) is a common adult-onset neurodegenerative disease characterized by the progressive death of motor neurons in the cerebral cortex, brain stem, and spinal cord. The exact mechanisms underlying the pathogenesis of ALS remain unclear. The current consensus regarding the pathogenesis of ALS suggests that the interaction between genetic susceptibility and harmful environmental factors is a promising cause of ALS onset. The investigation of putative harmful environmental factors has been the subject of several ongoing studies, but the use of transgenic animal models to study ALS has provided valuable information on the onset of ALS. Here, we review the current common invertebrate genetic models used to study the pathology, pathophysiology, and pathogenesis of ALS. The considerations of the usage, advantages, disadvantages, costs, and availability of each invertebrate model will also be discussed.

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Section: C Elegans Modelsmentioning

confidence: 99%

Invertebrate genetic models of amyotrophic lateral sclerosis

Zhou,

2024

Front. Mol. Neurosci.

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“…Aerosils 90, 200 and OX 50 that are used in cosmetics, drugs, food, inks, silicone rubber, tires and diverse plastic foils induced internal hatch at LOEL concentrations between 5 and 20 µg/mL. This clearly has ecotoxicological implications due to the growing distribution of nano silica and plastic foils in environmental sinks, such as soils or sediments, which represent natural habitats of wild C. elegans and similar nematodes [26,27]. (two-tailed Student's t-test).…”

Section: Silica Nanomaterials Induced the Behavior Defect Internal Hatchmentioning

confidence: 99%

Silica Nanoparticles Disclose a Detailed Neurodegeneration Profile throughout the Life Span of a Model Organism

Limke,

Poschmann,

Stühler

et al. 2024

JoX

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The incidence of age-related neurodegenerative diseases is rising globally. However, the temporal sequence of neurodegeneration throughout adult life is poorly understood. To identify the starting points and schedule of neurodegenerative events, serotonergic and dopaminergic neurons were monitored in the model organism C. elegans, which has a life span of 2–3 weeks. Neural morphology was examined from young to old nematodes that were exposed to silica nanoparticles. Young nematodes showed phenotypes such as dendritic beading of serotonergic and dopaminergic neurons that are normally not seen until late life. During aging, neurodegeneration spreads from specifically susceptible ADF and PDE neurons in young C. elegans to other more resilient neurons, such as dopaminergic CEP in middle-aged worms. Investigation of neurodegenerative hallmarks and animal behavior revealed a temporal correlation with the acceleration of neuromuscular defects, such as internal hatch in 2-day-old C. elegans. Transcriptomics and proteomics of young worms exposed to nano silica showed a change in gene expression concerning the gene ontology groups serotonergic and dopaminergic signaling as well as neuropeptide signaling. Consistent with this, reporter strains for nlp-3, nlp-14 and nlp-21 confirmed premature degeneration of the serotonergic neuron HSN and other neurons in young C. elegans. The results identify young nematodes as a vulnerable age group for nano silica-induced neural defects with a significantly reduced health span. Neurodegeneration of specific neurons impairs signaling by classical neurotransmitters as well as neuropeptides and compromises related neuromuscular behaviors in critical phases of life, such as the reproductive phase.

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“…Taken together, the list of C. elegans models for neuronal diseases is growing and getting more elaborate. The current invertebrate disease models are ready to elucidate the interactions between degeneration of distinct neurons, neuromuscular behaviors, age and environmental factors on a larger scale. , As outlined in the following sections, the study of genes, neurons and behavior along the entire life span of C. elegans may eventually close the evolutionary gap between nematode models and human disease by increasing our knowledge about the basic neurobiology of pollutant-induced neurodegeneration …”

Section: Elegans Models Of Neurodegenerative Aggregation Diseasesmentioning

confidence: 99%

Elegant Nematodes Improve Our Understanding of Human Neuronal Diseases, the Role of Pollutants and Strategies of Resilience

von Mikecz

2023

Environ. Sci. Technol.

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The prevalence of neurodegenerative disorders such as Alzheimer's and Parkinson's disease are rising globally. The role of environmental pollution in neurodegeneration is largely unknown. Thus, this perspective advocates exposome research in C. elegans models of human diseases. The models express amyloid proteins such as Aβ, recapitulate the degeneration of specifically vulnerable neurons and allow for correlated neurobehavioral phenotyping throughout the entire life span of the nematode. Neurobehavioral traits like locomotion gaits, rigidity, or cognitive decline are quantifiable and carefully mimic key aspects of the human diseases. Underlying molecular pathways of neurodegeneration are elucidated in pollutant-exposed C. elegans Alzheimer's or Parkinson's models by transcriptomics (RNA-seq), mass spectrometry-based proteomics and omics addressing other biochemical traits. Validation of the identified disease pathways can be achieved by genome-wide association studies in matching human cohorts. A consistent One Health approach includes isolation of nematodes from contaminated sites and their comparative investigation by imaging, neurobehavioral profiling and single worm proteomics. C. elegans models of neurodegenerative diseases are likewise wellsuited for high throughput methods that provide a promising strategy to identify resilience pathways of neurosafety and keep up with the number of pollutants, nonchemical exposome factors, and their interactions.

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Exposome, Molecular Pathways and One Health: The Invertebrate Caenorhabditis elegans

Cited by 5 publications

References 71 publications

Invertebrate genetic models of amyotrophic lateral sclerosis

Invertebrate genetic models of amyotrophic lateral sclerosis

Silica Nanoparticles Disclose a Detailed Neurodegeneration Profile throughout the Life Span of a Model Organism

Elegant Nematodes Improve Our Understanding of Human Neuronal Diseases, the Role of Pollutants and Strategies of Resilience

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