Natasha Vassileff

ORCID: 0000-0001-6554-4496
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About
Contact & Profiles
Research Areas
  • Extracellular vesicles in disease
  • Amyotrophic Lateral Sclerosis Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • RNA Research and Splicing
  • interferon and immune responses
  • Cholinesterase and Neurodegenerative Diseases
  • Protease and Inhibitor Mechanisms
  • Immune Response and Inflammation
  • Nanoplatforms for cancer theranostics
  • Inflammasome and immune disorders
  • Knee injuries and reconstruction techniques
  • Neurogenetic and Muscular Disorders Research
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Adenosine and Purinergic Signaling
  • MicroRNA in disease regulation
  • Total Knee Arthroplasty Outcomes
  • Fibromyalgia and Chronic Fatigue Syndrome Research

La Trobe University
2020-2024

Australian National University
2024

Small non-coding miRNA act as key regulators of several physiological processes due to their ability interact with numerous target mRNA within a network. Whilst can in concert regulate expression, miR-146a has emerged critical modulator inflammation by targeting upstream signalling proteins the nuclear factor kappa-light-chain-enhancer activated B cells (NF-κB) pathway and reductions this have been observed neurological neurodegenerative disorders. However, targeted assessment behaviour...

10.1016/j.mcn.2023.103820 article EN cc-by-nc-nd Molecular and Cellular Neuroscience 2023-02-01

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease characterized by the deposition of misfolded proteins in motor cortex and neurons. Although multitude ALS-associated mutated have been identified, several linked to small extracellular vesicles such as exosomes involved cell−cell communication. This study aims determine proteome isolated from ALS subjects identify novel deregulated proteins. Motor (MCEVs) were human postmortem (n = 10) neurological control (NC, n 5) brain...

10.3390/cells9071709 article EN cc-by Cells 2020-07-16

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease characterised by the deposition of aggregated proteins including TAR DNA-binding protein 43 (TDP-43) in vulnerable neurons and brain. Extracellular vesicles (EVs) facilitate spread neurodegenerative diseases can be easily accessed bloodstream. This study aimed to identify panel EV miRNAs that capture pathology occurring brain peripheral circulation. EVs were isolated from cortex (BDEVs) serum (serum EVs) 3 month-old...

10.1007/s12035-023-03857-z article EN cc-by Molecular Neurobiology 2024-01-22

Abstract Extracellular vesicles (EVs) are potentially useful biomarkers for disease detection and monitoring. Development of a label‐free technique imaging distinguishing small volumes EVs from different cell types states would be great value. Here, we have designed method to explore the chemical changes in associated with neuroinflammation using Time‐of‐Flight Secondary Ion Mass spectrometry (ToF‐SIMS) machine learning (ML). spectral was able identify differentiate released by microglia...

10.1002/jex2.110 article EN cc-by-nc-nd Journal of Extracellular Biology 2023-09-01

Abstract Neuroinflammation is an underlying feature of neurodegenerative conditions, often appearing early in the aetiology a disease. Microglial activation, prominent initiator neuroinflammation, can be induced through lipopolysaccharide (LPS) treatment resulting expression inducible form nitric oxide synthase (iNOS), which produces (NO). NO post‐translationally modifies cysteine thiols S‐nitrosylation, alter function target protein. Furthermore, packaging these NO‐modified proteins into...

10.1002/jev2.12455 article EN cc-by-nc-nd Journal of Extracellular Vesicles 2024-06-01

Abstract Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease characterized by the deposition of misfolded proteins leading to death motor neurons. Several ALS-associated proteins, including TAR DNA-binding protein 43 (TDP-43) and Superoxide dismutase-1 (SOD-1), have been linked small extracellular vesicles (EVs). However, role these EVs their cargo in ALS patients, prior treatment intervention, has not investigated. This study aims identify earliest changes facilitated...

10.1101/2023.07.26.23292854 preprint EN cc-by-nc-nd medRxiv (Cold Spring Harbor Laboratory) 2023-07-28

Abstract Neuroinflammation is initiated through microglial activation and cytokine release which can be induced lipopolysaccharide treatment (LPS) leading to a transcriptional cascade culminating in the differential expression of target proteins. These differentially expressed proteins then packaged into extracellular vesicles (EVs), form cellular communication, further propagating neuroinflammatory response over long distances. Despite this, EV proteome brain, following LPS treatment, has...

10.1002/jex2.165 article EN cc-by-nc-nd Journal of Extracellular Biology 2024-06-27
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