Maya K. Weigel

ORCID: 0000-0003-0557-5172
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Immune cells in cancer
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Galectins and Cancer Biology
  • Circadian rhythm and melatonin
  • Alzheimer's disease research and treatments
  • Glycosylation and Glycoproteins Research
  • Monoclonal and Polyclonal Antibodies Research
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Genetics and Neurodevelopmental Disorders
  • Amyotrophic Lateral Sclerosis Research
  • Neurological Disease Mechanisms and Treatments
  • Retinal and Optic Conditions
  • RNA regulation and disease
  • Immune Response and Inflammation

Stanford University
2020-2024

Palo Alto Institute
2022

Abstract Reactive astrocytes have been implicated in the pathogenesis of neurodegenerative diseases, including a non-cell autonomous effect on motor neuron survival ALS. We previously defined mechanism by which microglia release three factors, IL-1α, TNFα, and C1q, to induce neurotoxic astrocytes. Here we report that knocking out these factors markedly extends SOD1 G93A ALS mouse model, providing evidence for gliosis as potential therapeutic target.

10.1038/s41467-020-17514-9 article EN cc-by Nature Communications 2020-07-27

Glaucoma is a neurodegenerative disease that features the death of retinal ganglion cells (RGCs) in retina, often as result prolonged increases intraocular pressure. We show preventing formation neuroinflammatory reactive astrocytes prevents RGCs normally seen mouse model glaucoma. Furthermore, we these spared are electrophysiologically functional and thus still have potential value for function regeneration retina. Finally, demonstrate depends on combination both an injury to neurons...

10.1016/j.celrep.2020.107776 article EN cc-by Cell Reports 2020-06-01

Microglia and astrocytes play an important role in the neuroinflammatory response contribute to both destruction of neighboring tissue as well resolution inflammation following stroke. These reactive glial cells are highly heterogeneous at transcriptomic functional level. Depending upon stimulus, microglia mount a complex, specific composed distinct microglial astrocyte substates. substates ultimately drive landscape initiation recovery from adverse stimulus. In one state, inflammation-...

10.3389/fnmol.2023.1305949 article EN cc-by Frontiers in Molecular Neuroscience 2024-01-04

Abstract Microglia and astrocytes play an important role in the neuroinflammatory response contribute to both destruction of neighboring tissue as well resolution inflammation following stroke. These reactive glial cells are highly heterogeneous at transcriptomic functional level. Depending upon stimulus, microglia mount a complex, specific composed distinct microglial astrocyte substates. substates ultimately drive landscape initiation recovery from adverse stimulus. In one state,...

10.1101/2023.10.11.561918 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-10-16

2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) is an abundant constituent of central nervous system non-compact myelin, frequently used as a marker antigen for myelinating cells. The catalytic activity CNPase, the 3'-hydrolysis nucleotides, well characterised

10.1101/2024.05.25.595513 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-05-25

Abstract 2′,3′‐Cyclic nucleotide 3′‐phosphodiesterase (CNPase) is an abundant constituent of central nervous system non‐compact myelin, and its loss in mice humans causes neurodegeneration. Additionally, CNPase frequently used as a marker antigen for myelinating cells. The catalytic activity CNPase, the 3′‐hydrolysis 2′,3′‐cyclic nucleotides, well characterised vitro, but vivo function remains unclear. interacts with actin cytoskeleton to counteract developmental closure cytoplasmic channels...

10.1111/jnc.16274 article EN cc-by Journal of Neurochemistry 2024-12-10

Abstract Myelination depends on maintenance of oligodendrocytes that arise from oligodendrocyte precursor cells (OPCs). We show the dynamic nature oligodendroglia and myelination are regulated by circadian transcription factor BMAL1. Bmal1 knockdown in OPCs during development – but not adulthood decreases OPC proliferation, whereas BMAL1 regulates morphology throughout life. OPC-specific deficiency impairs remyelination an age-dependent manner, suggesting age-associated decrements regulation...

10.1101/2022.04.28.489946 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-04-30
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