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When telomeres reach a critical length, they can no longer bind sufficient telomere-capping proteins, exposing chromosome ends that activate DNA damage response (DDR) pathways [1]

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12,13,14,15,16,17 Unfortunately, for much of the subsequent 20th century, these concepts became superseded by the neurone doctrine, such that glial responses to CNS disorders were considered to be non-specific, stereotypic, always subsequent to primary neuronal damage and of little functional consequence