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This study developed a platform to prioritize Alzheimer's disease (AD) drug targets by filtering genes impacting mitochondrial and immune functions. Promising targets like Pdhb and Pdha1 were identified, showing potential for therapeutic development.

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Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Alzheimer's disease (AD) research generates many potential therapeutic targets from genetic and multi-omic studies.
  • Prioritizing these targets for drug development is challenging.
  • A new platform interprets systems-level risk signatures in AD patient data to form hypotheses.

Purpose of the Study:

  • To develop and validate a method for rapidly filtering candidate proteins.
  • To identify genes that can robustly modify targeted biological functions in vitro.
  • To validate hypotheses related to mitochondrial hypometabolism and chronic neuroinflammation in AD.

Main Methods:

  • Utilized mouse BV2 microglial cells and Psen2 knockdown cells.
  • Transfected cells with siRNA targeting 29 candidate genes.
  • Assessed mitochondrial function (Mitotracker TMRM, Alamar Blue) and immune function (pHrodo Green Zymosan, NF-κB reporter).
  • Analyzed proteomic effects of gene knockdown.

Main Results:

  • Several candidate genes impacted cellular phenotypes and proteomic signatures.
  • Identified targets reversing disease-associated proteomic signatures.
  • Psen2 knockdown sensitized cells, yielding more phenotypes and altered proteomic responses.
  • Highlighted Pdhb, Pdha1, Dlat, Ap2a2, and Psmc3 as promising targets modulating phenotypes and proteomic profiles.

Conclusions:

  • The developed approach effectively filters large sets of potential driver genes.
  • The method identifies genes capable of impacting targeted biological processes relevant to AD.
  • Validated targets will be prioritized for further resource development by the TREAT-AD consortium.