Chloe Allen

ORCID: 0000-0002-3333-7246
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About
Contact & Profiles
Research Areas
  • Amyotrophic Lateral Sclerosis Research
  • Neurogenetic and Muscular Disorders Research
  • Child Development and Digital Technology
  • Parkinson's Disease Mechanisms and Treatments
  • Immune cells in cancer
  • Urban, Neighborhood, and Segregation Studies
  • Autism Spectrum Disorder Research
  • Housing, Finance, and Neoliberalism
  • Digital Rights Management and Security
  • Mesenchymal stem cell research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Open Education and E-Learning
  • Biochemical Acid Research Studies
  • Homelessness and Social Issues
  • Adenosine and Purinergic Signaling
  • Amino Acid Enzymes and Metabolism
  • Copyright and Intellectual Property

University of Sheffield
2017-2024

As clinical evidence supports a negative impact of dysfunctional energy metabolism on the disease progression in amyotrophic lateral sclerosis, it is vital to understand how metabolic pathways are altered and whether they can be restored slow progression. Possible approaches include increasing or rerouting catabolism alternative fuel sources supplement glycolytic mitochondrial such as glycogen, ketone bodies nucleosides. To analyse basis catabolic defect sclerosis we used novel phenotypic...

10.1093/brain/awy353 article EN cc-by-nc Brain 2019-01-02

Amyotrophic lateral sclerosis (ALS) is characterised by motor neuron (MN) death; however, astrocytes play a key role in disease pathogenesis. Developments the field of artificial intelligence (AI) have potential to impact drug discovery multiple ways, including rapid identification repurposing candidates. A combination natural language processing and deep learning algorithms was used generate knowledge graph based on scientific literature, omics chemical databases, other public sources with...

10.1101/2025.03.06.641147 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2025-03-10

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative condition for which new therapeutic options are urgently needed. We injected GFP+ adipose-derived stem cells (EGFP-ADSCs) directly into the cerebrospinal fluid (CSF) of transgenic SOD1G93A mice, well-characterized model familial ALS. Despite short-term survival and limited engraftment efficiency, EGFP-ADSCs improved motor function delayed disease onset by promoting neuron (MN) reducing glial activation. then tested in...

10.1016/j.omtm.2021.03.017 article EN cc-by-nc-nd Molecular Therapy — Methods & Clinical Development 2021-03-27

Abstract: M102 is a central nervous system (CNS) penetrant small molecule electrophile which activates in vivo the NFE2-related factor 2 antioxidant response element (NRF2-ARE) pathway, as well transcription of heat-shock (HSE) associated genes. In TDP-43Q331K transgenic mouse model ALS dosed subcutaneously at 5mg/kg OD or 2.5mg/kg BD with M102, significant improvements compound muscle action potential (CMAP) amplitude hind limb muscles and gait parameters were observed 6 months age, target...

10.1101/2024.12.08.627389 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-12-14
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