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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: J Neurol Neuromedicine. 2016 Sep;1(3):17–22. doi: 10.29245/2572.942x/2016/3.1016

Figure 1.

Figure 1

Schematic presentation of a potential link of DSB, DNA-PK and Aβ in AD brains. Upon induction of DSB either by normal aging/ROS or other DNA damaging agents, Ku80/Ku70 and DNA-PKcs are rapidly recruited to DNA ends, and DNA repair occurs as it would in normal cases. However, in AD brains, in addition to formation of Aβ oligomers from Aβ peptides, sustained DSB in the genome would cause genome instability leading to the loss of normal neuronal activity. Additionally, with depleted Ku80, a somatostatin receptor, disruption of somatostatin signaling could potentially induce Aβ generation thus accelerating AD pathology.

DSB: DNA double strand break; DNA-PK: DNA-dependent protein kinase; ROS: Reactive oxygen species; Aβ Amyloid beta