![]() Because of their importance in public health, it is necessary to study the causes, diagnosis methods and possible treatments of this pathology. According to the World Alzheimer’s report, this pathology comprises over the 60% of all causes of dementia, and they estimate that there are around 46.8 million people living with the disease at 2015. AD patients present a deficiency in short‐term memory and problem‐solving skills, affecting his daily activities and quality of life. In this chapter, we analyse current evidence that suggests that mitochondrial injury is an important factor in the pathogenesis of AD and how studying this process could reveal new strategies to mitigate neurodegeneration and to develop new diagnostic methods for an early detection of AD.Īlzheimer’s disease (AD) is a complex and irreversible neurodegenerative disorder characterized by a progressive memory and cognitive impairment. ![]() Interestingly, the examination of peripheral cells from AD patients also presents mitochondrial dysfunction, suggesting that tracking these mitochondrial defects in peripheral cells could be a potential mechanism of early diagnosis of AD. Therefore, reducing mitochondrial injury may have beneficial effects for neuronal dysfunction and cognitive decline observed in AD patients. In this scenario, accumulative evidence suggests that mitochondrial dysfunction precedes the establishment of tau and Aβ pathology and contributes to synaptic degeneration observed in AD. AD principally affects the memory and cognitive functions of the patients, and currently, successful strategies for diagnosis and early treatment are lacking. Evidence suggests that these elements affect neurons compromising energy supply, antioxidant response and synaptic activity. AD is characterized by brain presence of senile plaques, which are formed by aggregates of Aβ peptide and neurofibrillary tangles (NFTs), formed by pathological forms of tau protein. Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia. ![]()
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