Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia. 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. Evidence suggests that these elements affect neurons compromising energy supply, antioxidant response and synaptic activity. AD principally affects the memory and cognitive functions of the patients, and currently, successful strategies for diagnosis and early treatment are lacking. 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. Therefore, reducing mitochondrial injury may have beneficial effects for neuronal dysfunction and cognitive decline observed in AD patients. 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. 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.
Part of the book: Update on Dementia
Ethanol is a licit drug consumed by a large part of the population, from adolescence to adulthood. High ethanol consumption is a public health problem due to its addictiveness and the risk it produces of developing other diseases, including cardiovascular, hepatic, and mental pathologies. Different patterns of ethanol consumption and its toxic effects in the brain have been reported. Current studies suggest to mitochondria, one of the principal mediators for ethanol neurotoxicity. In this chapter, we will review the effects of ethanol on neurons in different scenarios of ethanol consumption and its relation with mitochondrial function. Finally, we will propose a mechanism of ethanol toxicity in which the mitochondria are the main mediator and in which the mitochondrial alterations correlate with the severity of ethanol consumption. Thus, improving mitochondrial health of brain cells could be considered as a potential therapeutic target to treat ethanol-associated disorders.
Part of the book: Mitochondrial Diseases