NDUFS2: A Target Enabling Package

The molecular role of NDUFS2 in mitochondrial metabolism is through its participation in complex I of the respiratory chain within the inner membrane of mitochondria.  Complex I function is critical for mitochondrial ATP production, but is also involved in reactive oxygen species production.  As a core component of complex I, NDUFS2 resides within two hypotheses of opposing mechanisms with the potential to foster AD pathology: AD Hypometabolism Hypothesis and the AD Oxidative Stress Hypothesis.  Each hypothesis is subordinate to a separately identified biological domain (mitochondrial metabolism and oxidative stress).  Consequently, decreasing complex I integrity via down-regulation of NDUFS2 could either promote or decrease the propagation of AD pathology.  The primary aim of this project is to generate resources to more effectively study the role of NDUFS2 in AD pathogenesis, through the generation of a basic TEP suite of resources, including a full antibody characterization report linked below.  Future studies leveraging these resources may shed light onto the molecular mechanism associated with NDUFS2 linkage with AD risk.