proportion between ADAD and LOAD are not driven by TREM2 carrier brains. Based on our results, we would hypothesize that this change in Aβ processing of ADAD would lead to more direct to neuronal death than the pathological processes of LOAD. Similarly, decreased neuronal and increased astrocyte relative proportions were significantly associated with APOE ε4 allele. It has been reported APOE ε4 allele increases the risk for AD by affecting APP metabolism or Aβ clearance [69, 70], suggesting a direct link between APP metabolism and neuronal death.
