Mitochondrial Gatekeeper TOM70: A Potential Alzheimer’s Biomarker

Published on November 2, 2022

Imagine the translocase of the outer membrane (TOM) complex as the doorman of the mitochondria, allowing only the right tenants in. In Alzheimer’s disease (AD), this doorman, specifically TOM70, seems to be less diligent in its duties. Researchers found reduced levels of TOM70 in both the blood and hippocampus of mouse models with AD. They also analyzed blood samples from patients with AD, dementia with Lewy bodies (DLB), and post-stroke dementia (PSD) and discovered that TOM70 mRNA levels were decreased in AD patients and correlated with disease progression. This suggests that the expression of TOM70 could serve as a potential biomarker for AD diagnosis and monitoring the progression of the disease. With further research, scientists hope to unlock the full potential of TOM70 as a gatekeeper predicting the impact of mitochondrial dysfunction in Alzheimer’s.

Mitochondrial dysfunction plays a key role in the pathogenesis of Alzheimer’s disease (AD). The translocase of the outer membrane (TOM) complex controls the input of mitochondrial precursor proteins to maintain mitochondrial function under pathophysiological conditions. However, its role in AD development remains unclear. TOM70 is an important translocase present in the TOM complex. In the current study, we found that TOM70 levels were reduced in the peripheral blood and hippocampus of the APP/PS1 mice. In addition, we examined the whole-blood mRNA levels of TOM70 in patients with AD, dementia with Lewy bodies (DLB), and post-stroke dementia (PSD). Our study revealed that the mRNA level of TOM70 was decreased in the blood samples of patients with AD, which was also correlated with the progression of clinical stages. Therefore, we proposed that the expression of TOM70 could be a promising biomarker for AD diagnosis and monitoring of disease progression.

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