A5013021051- Sirtuins and Resveratrol in Medicine
- Nerve injury and regeneration
- Signaling Pathways in Disease
- Calpain Protease Function and Regulation
- Axon Guidance and Neuronal Signaling
- Genetics, Aging, and Longevity in Model Organisms
- Cholinesterase and Neurodegenerative Diseases
- Calcium signaling and nucleotide metabolism
- Genomics, phytochemicals, and oxidative stress
- RNA and protein synthesis mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Curcumin's Biomedical Applications
- Neuroinflammation and Neurodegeneration Mechanisms
- Toxoplasma gondii Research Studies
- Machine Learning in Bioinformatics
- Neurobiology and Insect Physiology Research
- RNA regulation and disease
University of Lausanne
2020-2024
Institute of Biosciences and Bioresources
2016-2020
National Research Council
2016-2020
Axon degeneration contributes to the disruption of neuronal circuit function in diseased and injured nervous systems. Severed axons degenerate following activation an evolutionarily conserved signaling pathway, which culminates SARM1 mammals execute pathological depletion metabolite NAD+. NADase activity is activated by NAD+ precursor nicotinamide mononucleotide (NMN). In mammals, keeping NMN levels low potently preserves after injury. However, it remains unclear whether also a key mediator...
Common copathogenic factors, including oxidative stress and neuroinflammation, are found to play a vital role in the development of neurodegenerative disorders, Alzheimer's disease (AD) Parkinson's (PD). Nowadays, owing multifactorial character diseases, no effective therapies available, thus underlying need for new strategies. Overexpression enzyme GSK-3β downregulation Nrf2/ARE pathway responsible decrease antioxidant defense effects. These pieces evidence underline usefulness dual...
Dopamine transporter deficiency syndrome (DTDS) is a novel autosomal recessive disorder caused by mutations in the dopamine (DAT), which leads to partial or total loss of function protein. DTDS pharmacoresistant and very little known about its neurobiology, part due lack relevant animal models. The objective this study was establish first model for with strong construct validity, using Caenorhabditis elegans, investigate vivo role played DTDS-related found human DAT (hDAT). We took advantage...
Axon degeneration is a shared feature in neurodegenerative disease and when nervous systems are challenged by mechanical or chemical forces. However, our understanding of the molecular mechanisms underlying axon remains limited. Injury-induced serves as simple model to study how severed axons execute their own disassembly (axon death). Over recent years, an evolutionarily conserved death signaling cascade has been identified from flies mammals, which required for separated degenerate after...
Axon degeneration is a shared feature in neurodegenerative disease and when nervous systems are challenged by mechanical or chemical forces. However, our understanding of the molecular mechanisms underlying axon remains limited. Injury-induced serves as simple model to study how severed axons execute their own disassembly (axon death). Over recent years, an evolutionarily conserved death signaling cascade has been identified from flies mammals, which required for separated degenerate after...
Abstract After injury, the severed axon separated from soma activates programmed degeneration, an evolutionarily conserved pathway to initiate its degeneration within a day. Conversely, projections deficient in remain morphologically preserved with functional synapses for weeks months after injury. How this synaptic function is sustained remains currently unknown. Here, we demonstrate that dNmnat-mediated over-expression attenuates distinct neuronal populations. Severed When evoked, they...
Abstract Axon degeneration contributes to the disruption of neuronal circuit function in diseased and injured nervous systems. Severed axons degenerate following activation an evolutionarily conserved signaling pathway, which culminates SARM1 mammals execute pathological depletion metabolite NAD + . NADase activity is activated by precursor nicotinamide mononucleotide (NMN). In mammals, keeping NMN levels low potently preserves after injury, however, it remains unclear whether also a key...