Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update

Mol Neurobiol. 2024 Feb 17. doi: 10.1007/s12035-024-04009-7. Online ahead of print.

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease characterized by memory impairment and a progressive decline in cognitive function. Mitochondrial dysfunction has been identified as an important contributor to the development of AD, leading to oxidative stress and energy deficits within the brain. While current treatments for AD aim to alleviate symptoms, there is an urgent need to target the underlying mechanisms. The emerging field of mitotherapy, which involves the transplantation of healthy mitochondria into damaged cells, has gained substantial attention and has shown promising results. However, research in the context of AD remains limited, necessitating further investigations. In this review, we summarize the mitochondrial pathways that contribute to the progression of AD. Additionally, we discuss mitochondrial transfer among brain cells and mitotherapy, with a focus on different administration routes, various sources of mitochondria, and potential modifications to enhance transplantation efficacy. Finally, we review the limited available evidence regarding the immune system's response to mitochondrial transplantation in damaged brain regions.

Keywords: Alzheimer’s disease; Energy metabolism; Mitochondria; Mitochondrial transplantation; Neurodegenerative diseases.

Publication types

  • Review