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• W2000251938 abstract "Neurodegenerative disorders of aging represent a growing public health concern. In the United States alone, there are now >5 million patients with Alzheimer’s disease (AD), the most common form of dementia. No therapeutic approaches are available that alter the relentless course of AD or other dementias of aging. A major hurdle to the development of effective therapeutics has been the lack of predictive model systems in which to develop and validate candidate therapies. Animal model studies based on the analysis of transgenic mice that overexpress rare familial AD-associated mutant genes have been informative about mechanisms of familial disease, but they have not proven predictive for drug development. New approaches to disease modeling are of particular interest. Methods such as epigenetic reprogramming of patient skin fibroblasts to human induced pluripotent stem cells, which can be differentiated into patient-derived neuron subtypes, have generated significant excitement because of their potential to model more accurately aspects of human neurodegeneration. Studies focused on the generation of human neuron models of AD and frontotemporal dementia have pointed to pathologic pathways and potential therapeutic venues. This article discusses the promise and potential pitfalls of modeling of dementia disorders based on somatic cell reprogramming. Neurodegenerative disorders of aging represent a growing public health concern. In the United States alone, there are now >5 million patients with Alzheimer’s disease (AD), the most common form of dementia. No therapeutic approaches are available that alter the relentless course of AD or other dementias of aging. A major hurdle to the development of effective therapeutics has been the lack of predictive model systems in which to develop and validate candidate therapies. Animal model studies based on the analysis of transgenic mice that overexpress rare familial AD-associated mutant genes have been informative about mechanisms of familial disease, but they have not proven predictive for drug development. New approaches to disease modeling are of particular interest. Methods such as epigenetic reprogramming of patient skin fibroblasts to human induced pluripotent stem cells, which can be differentiated into patient-derived neuron subtypes, have generated significant excitement because of their potential to model more accurately aspects of human neurodegeneration. Studies focused on the generation of human neuron models of AD and frontotemporal dementia have pointed to pathologic pathways and potential therapeutic venues. This article discusses the promise and potential pitfalls of modeling of dementia disorders based on somatic cell reprogramming. Neurodegenerative Dementias: Connecting Psychiatry and Neurology Through a Shared NeurobiologyBiological PsychiatryVol. 75Issue 7PreviewIt is becoming increasingly hard to ignore the fact that as we improve medical treatment of common diseases and extend the human life span, we face an epidemic of dementia, which poses a terrible burden on society at all levels. Identifying disease course–altering treatments for dementia has become an imperative not only for neurologists, psychiatrists, and other medical professionals but also for humanity as a whole. This issue of Biological Psychiatry presents eight reviews from leading experts who provide authoritative analyses of their respective areas, offering a broad overview of the current state of research in dementia. Full-Text PDF" @default.
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• W2000251938 date "2014-04-01" @default.
• W2000251938 modified "2023-10-18" @default.
• W2000251938 title "Dementia in a Dish" @default.
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• W2000251938 doi "https://doi.org/10.1016/j.biopsych.2014.01.007" @default.
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