Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update.
Pegah JavadpourFatemeh AbbaszadehAbolhassan AhmadianiMohsen RezaeiRasoul GhasemiPublished in: Molecular neurobiology (2024)
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.
Keyphrases
- oxidative stress
- induced apoptosis
- resting state
- immune response
- cell cycle arrest
- white matter
- working memory
- cell death
- ischemia reperfusion injury
- diabetic rats
- dna damage
- cognitive decline
- multiple sclerosis
- cell therapy
- functional connectivity
- endoplasmic reticulum stress
- reactive oxygen species
- stem cells
- depressive symptoms
- dendritic cells
- risk assessment
- drinking water
- inflammatory response
- human health
- heat shock protein