Mitochondrial SOS: how mtDNA may act as a stress signal in Alzheimer’s disease

Abstract

Background Alterations in mitochondrial DNA (mtDNA) levels have been observed in Alzheimer’s disease and are an area of research that shows promise as a useful biomarker. It is well known that not only are the mitochondria a key player in producing energy for the cell, but they also are known to interact in other important intracellular processes as well as extracellular signaling and communication. Body This mini review explores how cells use mtDNA as a stress signal, particularly in Alzheimer’s disease. We investigate the measurement of these mtDNA alterations, the mechanisms of mtDNA release, and the immunological effects from the release of these stress signals. Conclusion Literature indicates a correlation between the release of mtDNA in Alzheimer’s disease and increased immune responses, showing promise as a potential biomarker. However, several questions remain unanswered and there is great potential for future studies in this area.

The Role of Mitochondrial Copy Number in Neurodegenerative Diseases: Present Insights and Future Directions

“…It is known that neurodegenerative processes can start before the appearance of clinical manifestations, and alteration in mtDNA-CN may be the sign of initial cognitive decline [ 34 ]. All these findings support the contribution of mtDNA-CN as a candidate biomarker in the pathogenesis of neurodegeneration, even in the early stages of disease, because its alteration could reflect mitochondrial biogenesis and function.…”