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Regardless of the specific protein/mechanism compromised, we believe that HSV-1-induced accumulation of DSBs in neuronal genome might induce neurodegeneration through different pathways (i.e., p53-mediated apoptosis, autophagy deficiency and cell cycle re-entry), as observed in AD (Roos and Kaina, Overall, our data indicate that HSV-1 productive infection causes an impairment of NHEJ pathway and DNA damage accumulation in primary neurons

Additionally, they exert a neuroprotective effect independently of blood glucose levels ( Table 2 )