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Additionally, the accumulation of senescent glial and neuronal cells has been shown to drive the senescence-associated secretory phenotype (SASP), further amplifying inflammation and oxidative damage

during chromosome replication, DNA-replicating enzymes cannot continue replication to the very end of the chromosome, so with each replication the chromosome end is shortened (this is because the synthesis of fragments requires the attachment of RNA primers to the lagging strand)

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