The role of mitochondrial dysfunction in Alzheimer's disease: A potential pathway to treatment

Is Mitochondria DNA Variation a Biomarker for AD?

“…Mitochondria are responsible for producing energy, detoxifying, communicating between brain cells, regulating temperature and keeping the redox balance of the cells [ 11 , 12 ]. In neurons, mitochondria participate in nerve signaling by maintaining neuron membrane potential.…”

“…In neurons, mitochondria participate in nerve signaling by maintaining neuron membrane potential. Most ATP consumed by the central nervous system (CNS) is supplied by oxidative metabolism, causing neurons fully rely on the normal function of mitochondria [ 11 ]. Recent studies have shown that mitochondrial dysfunction and increased oxidative stress are common features of AD and probably participate in the pathogenesis of AD, although the underlying mechanism is controversial [ 13 ].…”

Acetylated Tau Protein: A New Piece in the Puzzle between Brain Ischemia and Alzheimer’s Disease

“…There is growing awareness and a realization of the challenges faced by different countries as the proportion of population living with symptoms of dementia continues to grow. Despite a large amount of research into the causes and processes leading to dementia and numerous projects to look for therapies modifying the progress of dementia that will have a decisive impact on neurodegeneration after ischemia and the development of Alzheimer’s disease, there has still been no breakthrough [ 27 , 28 , 29 ]. Moreover, drug failures affecting the progression of dementia are not optimistic at the moment.…”

“…Ischemic brain damage and Alzheimer’s disease lead to the death of neurons, which drastically reduces their number in the neuronal network, adversely affecting the elderly who already have a reduced number of neurons due to aging. Due to the lack of causal treatment of brain ischemia and Alzheimer’s disease [ 27 , 28 , 29 ], it is advisable to investigate, compare and search for similarities in the development and pathological processes occurring in both neuropathological units. This is particularly relevant when new data indicate that ischemic mechanisms may take part in the development of Alzheimer’s disease and that there is a similarity of molecular phenomena between brain post-ischemic neurodegeneration and Alzheimer’s disease [ 1 , 3 , 4 , 5 ].…”

“…The disease affects more than 40 million patients worldwide, and the incidence of Alzheimer’s disease doubles every five years after the age of 65 [ 77 ]. The established failure of anti-amyloid therapy with the intention of changing the course of Alzheimer’s disease in clinical trials has led to a radical change in thinking about the etiopathogenesis of the disease [ 27 , 28 , 29 ]. This situation has directed a group of scientists to brain ischemia, which, like Alzheimer’s disease, mainly has changes in the hippocampus.…”