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Clarifying regulatory mechanisms and targeting biomarkers of CSCs is currently the mainstream idea

For instance, the M83 mouse expressing mutant human syn demonstrates that abnormal syn accumulation is sufficient to drive neurodegenerative phenotypes including neuronal hyperactivity and vascular patterning defects, even in the absence of overt systemic inflammation [164, 165]

Conversely, histone deacetylases (HDACs) remove acetyl groups, leading to chromatin condensation and gene repression

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