Alzheimer's Disease (AD) is the most prevalent form of dementia and is characterized by progressive memory loss and cognitive decline. The underlying mechanism of AD has not been fully understood. At present there is no method to detect AD at its early stage. Recent studies indicate that mitochondria dysfunction is related to AD pathogenesis. Altered mitochondria functions are found in AD and influence both amyloid-β (Aβ) and tau pathology. Variations in mitochondria DNA (mtDNA) lead to a change in energy metabolism in the brain and contribute to AD. MtDNA can reflect the status of mitochondria and therefore play an essential role in AD. In this review, we summarize the changes in mtDNA and mtDNA mutations in AD patients and discuss the possibility of mtDNA being a biomarker for the early diagnosis of AD.
Keyphrases
- cognitive decline
- mitochondrial dna
- early stage
- copy number
- cell death
- mild cognitive impairment
- reactive oxygen species
- multiple sclerosis
- squamous cell carcinoma
- newly diagnosed
- single molecule
- gene expression
- cognitive impairment
- cell free
- blood brain barrier
- patient reported outcomes
- functional connectivity
- lymph node
- prognostic factors
- chronic kidney disease
- nucleic acid
- rectal cancer
- circulating tumor cells
- patient reported