We are analyzing https://link.springer.com/article/10.1007/s12031-024-02227-1.

Title:
Aneuploidy is Linked to Neurological Phenotypes Through Oxidative Stress | Journal of Molecular Neuroscience
Description:
Aneuploidy, having an aberrant genome, is gaining increasing attention in neurodegenerative diseases. It gives rise to proteotoxic stress as well as a stereotypical oxidative shift which makes these cells sensitive to internal and environmental stresses. A growing body of research from numerous laboratories suggests that many neurodegenerative disorders, especially Alzheimer’s disease and frontotemporal dementia, are characterised by neuronal aneuploidy and the ensuing apoptosis, which may contribute to neuronal loss. Using Drosophila as a model, we investigated the effect of induced aneuploidy in GABAergic neurons. We found an increased proportion of aneuploidy due to Mad2 depletion in the third-instar larval brain and increased cell death. Depletion of Mad2 in GABAergic neurons also gave a defective climbing and seizure phenotype. Feeding animals an antioxidant rescued the climbing and seizure phenotype. These findings suggest that increased aneuploidy leads to higher oxidative stress in GABAergic neurons which causes cell death, climbing defects, and seizure phenotype. Antioxidant feeding represents a potential therapy to reduce the aneuploidy-driven neurological phenotype.
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Keywords {🔍}

pubmed, aneuploidy, article, google, scholar, cas, cell, brain, central, disease, neurons, drosophila, neurological, climbing, stress, alzheimers, mad, death, increased, control, cells, neuronal, flies, phenotype, oxidative, phenotypes, defects, diseases, depletion, neurodegenerative, gabaergic, seizure, aneuploid, feeding, iourov, yurov, chromosome, adult, disorders, fig, neurogenesis, model, wildtype, mol, analysis, shaukat, chromosomal, repeat, larval, dna,

Topics {✒️}

central nervous system low-level post-zygotic aneuploidy article download pdf dino-lite digital microscope genome-damaged cells safeguards dosage-compensated aneuploids relative unaffected aged-matched controls writing—original draft preparation mad2-depleted larval brains ki67 phospho-protein expression gov/pubmed/9176387 migliore bang-sensitive behavioural assays elevated beta-secretase expression hypoxia-induced cell death clarify genetic-environmental interactions mad2-depleted larval brain gad1-gal4 driver visualised mad2-depleted flies compared bang-sensitivity behavioural assay wild-type larval brain n-acetylcysteine amide chromosome mis-segregation instar larval brains privacy choices/manage cookies free radical formation remain post-mitotic amyloid beta peptide normal climbing ability polyalanine repeat sequence 100 µg/ml naca feeding aneuploidy-driven neurological phenotype age-related neurodegenerative diseases age-related metabolic disorders gabaergic neuron increased spalding kl yurov yb instar larval brain induce neuronal aneuploidy pre-existing neurons stem cell biology article islam wild-type control flies related subjects garcia-verdugo jm medical research institute naca feeding showed climbing defects compared 500 ml measuring cylinder increased oxidative stress spindle assembly checkpoint

Questions {❓}

Arendt T, Stieler J, Ueberham U (2017) Is sporadic Alzheimer’s disease a developmental disorder?
Neuronal hyperexcitability in Alzheimer’s disease: what are the drivers behind this aberrant phenotype?
Vincent I, Rosado M, Davies P (1996) Mitotic mechanisms in Alzheimer’s disease?

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         description:Aneuploidy, having an aberrant genome, is gaining increasing attention in neurodegenerative diseases. It gives rise to proteotoxic stress as well as a stereotypical oxidative shift which makes these cells sensitive to internal and environmental stresses. A growing body of research from numerous laboratories suggests that many neurodegenerative disorders, especially Alzheimer’s disease and frontotemporal dementia, are characterised by neuronal aneuploidy and the ensuing apoptosis, which may contribute to neuronal loss. Using Drosophila as a model, we investigated the effect of induced aneuploidy in GABAergic neurons. We found an increased proportion of aneuploidy due to Mad2 depletion in the third-instar larval brain and increased cell death. Depletion of Mad2 in GABAergic neurons also gave a defective climbing and seizure phenotype. Feeding animals an antioxidant rescued the climbing and seizure phenotype. These findings suggest that increased aneuploidy leads to higher oxidative stress in GABAergic neurons which causes cell death, climbing defects, and seizure phenotype. Antioxidant feeding represents a potential therapy to reduce the aneuploidy-driven neurological phenotype.
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      headline:Aneuploidy is Linked to Neurological Phenotypes Through Oxidative Stress
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