January 11

Hot Off the Press: Mitochondrial translocase of the outer membrane (TOM) alterations may underlie dysfunctional oxidative phosphorylation in Alzheimer’s disease

The translocase of the outer membrane (TOM) is a vital mitochondrial transport system facilitating the importation of nuclear encoded proteins into the organelle. While mitochondrial dysfunction, including perturbation of oxidative phosphorylation (OXPHOS) complex, is evident in Alzheimer’s disease (AD), it remains unclear whether the observed OXPHOS deficits may be associated with TOM alterations. In this study, the objective was to correlate TOM subunits with OXPHOS complex proteins in AD. We used postmortem neocortex (BA40) from AD and age-matched controls were processed to obtain mitochondrial enriched homogenates for the measurement of Tom20, Tom22, Tom40, Tom70 as well as components of OXPHOS complex I – V by immunoblotting. We found that Tom20 and Tom70 immunoreactivities were significantly reduced in AD, as were components of OXPHOS complex I and III. Both Tom20 and Tom70 positively correlated with complex III and V, while Tom20 also correlated with complex IV. In conclusion, reductions in certain TOM subunits and their correlations with specific OXPHOS complex proteins suggest that an impaired mitochondrial transportation system may contribute to previously observed oxidative phosphorylation deficits in AD. Follow-up studies are needed to corroborate the present correlative study.


Atamna H, Frey WH, 2nd (2007) Mechanisms of mitochondrial dysfunction and energy deficiency in Alzheimer’s disease. Mitochondrion 7:297-310.

Chai YL, Xing H, Chong JR et al. (This paper).

© 2014 Lai Lab, NUS. All rights reserved.

Posted January 11, 2018 by Mitchell Lai in category Dementia Neurochemistry, Hot Off the Press