Researchers discovered that oligodendrocytes, not just neurons, produce amyloid β in Alzheimer's disease, and suppressing their activity improves disease pathology. This finding suggests new therapeutic targets for Alzheimer's treatment.
By Dr. Chinta SidharthanReviewed by Susha Cheriyedath, M.Sc.Jul 24 2024 In a recent study published in the journal PLOS Biology, researchers used mouse models to demonstrate that neurons were not the only source of abnormal amyloid β proteins contributing to the pathology of Alzheimer's disease. They found that oligodendrocytes play a significant role in the abnormal neuronal hyperactivity in Alzheimer's disease and are a major source of amyloid β protein.
One of the first neuronal responses to the accumulation of amyloid β plaques is increased and abnormal excitability. Transcriptomics-based research has shown that astrocytes, microglia, and oligodendrocytes in mouse models of Alzheimer's disease and Alzheimer's disease tissue from humans show abnormal responses to amyloid β.
Post-mortem tissue from patients who had sporadic Alzheimer's disease, as well as from healthy controls, were used for in-situ hybridization and RNA scoping to determine whether Alzheimer's disease altered the amyloid β-producing capacity of oligodendrocytes.
The study also compared the amyloid β production between oligodendrocytes and neurons by producing cortical neurons from the same pluripotent stem cells used to derive oligodendrocytes and examining the production of amyloid β in both cell lines. Results The study found that not only do oligodendrocytes produce greater amounts of amyloid β than neurons, but also contribute significantly to the abnormal neuronal hyperactivity observed in Alzheimer's disease. Furthermore, selective suppression of amyloid β production in the oligodendrocytes was found to improve Alzheimer's disease pathology.
Antibodies Cell Cortex Genes Hyperactivity In Vivo Microglia Nervous System Neurons Pathology Pathophysiology Protein Research RNA Stem Cells Transcriptomics
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