With a constantly increasing aging population, neurocognitive diseases are emerging as a worldwide problem affecting not only their patients but also the people who care for them, putting pressure on healthcare systems and the economy as a whole. Despite the enormous research efforts and many clinical trials, Alzheimer's disease, the leading form of dementia, has to date no effective drugs to slow the progression of, or to treat the disease. Notably, early diagnosis of Alzheimer's disease and other neurocognitive disorders, even before the first signs of dementia appear, is thought to be key in preventing the progression of the disease. Furthermore, it has been suggested that many drugs in clinical trials fail to show efficacy as they are tested in patients with advanced forms of dementia. Thus, early diagnosis of neurocognitive disorders is equally important as effective treatments. Identifying and targeting complex pathological mechanisms for treatment or diagnosis is vital in neurocognitive diseases. Although the mechanism of the pathogenesis of neurocognitive disorders remain unknown, recent evidence highlights that mitochondrial dysfunction plays an essential role in the pathophysiology of these diseases. Thus, elucidating the role of mitochondria in the development and progression of this group of diseases could lead to alternative therapeutic treatments.
Many hypotheses for the pathogenesis of cognitive disorders, including Alzheimer's disease, have been put forward, and many more dysfunctional individual cellular processes have been associated with these hypotheses. Dysfunctional mitochondria are thought to play a vital role in these diseases as healthy mitochondria not only support neuronal activity by providing energy, but also protect the neurons from oxidative damage and are crucial in apoptosis. Recent evidence implicates mitochondrial dysfunction as a common mechanism along with many well-established pathological mechanisms, such as the formation of amyloid-beta (Aß) aggregates, neurofibrillary tangles, impaired synaptic transmission, oxidative stress, neurodegeneration and neuroinflammation. In this regard, exploring the mitochondrial processes that are altered during the pathogenesis of neurocognitive diseases, such as structural and functional changes, may offer promising therapeutic targets for cognitive-related disease diagnosis and treatment.
This Research Topic aims to gather manuscripts (review papers or original research articles) that study mitochondria dysfunction in Alzheimer's disease or other cognitive declining diseases such as Huntington's, Lewy Body and Parkinson's disease. We welcome the submission of papers focusing on mitochondrial dysfunction to target or diagnose these diseases including in silico in-vitro, and in-vivo studies including experimental therapeutics. Overall, this topic will address mitochondria dysfunction and gather information on new targets, new therapeutics, and potential novel biomarkers of cognitive diseases.
With a constantly increasing aging population, neurocognitive diseases are emerging as a worldwide problem affecting not only their patients but also the people who care for them, putting pressure on healthcare systems and the economy as a whole. Despite the enormous research efforts and many clinical trials, Alzheimer's disease, the leading form of dementia, has to date no effective drugs to slow the progression of, or to treat the disease. Notably, early diagnosis of Alzheimer's disease and other neurocognitive disorders, even before the first signs of dementia appear, is thought to be key in preventing the progression of the disease. Furthermore, it has been suggested that many drugs in clinical trials fail to show efficacy as they are tested in patients with advanced forms of dementia. Thus, early diagnosis of neurocognitive disorders is equally important as effective treatments. Identifying and targeting complex pathological mechanisms for treatment or diagnosis is vital in neurocognitive diseases. Although the mechanism of the pathogenesis of neurocognitive disorders remain unknown, recent evidence highlights that mitochondrial dysfunction plays an essential role in the pathophysiology of these diseases. Thus, elucidating the role of mitochondria in the development and progression of this group of diseases could lead to alternative therapeutic treatments.
Many hypotheses for the pathogenesis of cognitive disorders, including Alzheimer's disease, have been put forward, and many more dysfunctional individual cellular processes have been associated with these hypotheses. Dysfunctional mitochondria are thought to play a vital role in these diseases as healthy mitochondria not only support neuronal activity by providing energy, but also protect the neurons from oxidative damage and are crucial in apoptosis. Recent evidence implicates mitochondrial dysfunction as a common mechanism along with many well-established pathological mechanisms, such as the formation of amyloid-beta (Aß) aggregates, neurofibrillary tangles, impaired synaptic transmission, oxidative stress, neurodegeneration and neuroinflammation. In this regard, exploring the mitochondrial processes that are altered during the pathogenesis of neurocognitive diseases, such as structural and functional changes, may offer promising therapeutic targets for cognitive-related disease diagnosis and treatment.
This Research Topic aims to gather manuscripts (review papers or original research articles) that study mitochondria dysfunction in Alzheimer's disease or other cognitive declining diseases such as Huntington's, Lewy Body and Parkinson's disease. We welcome the submission of papers focusing on mitochondrial dysfunction to target or diagnose these diseases including in silico in-vitro, and in-vivo studies including experimental therapeutics. Overall, this topic will address mitochondria dysfunction and gather information on new targets, new therapeutics, and potential novel biomarkers of cognitive diseases.
