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7.342 The Biology of Aging: Age-Related Diseases and Interventions (MIT) 7.342 The Biology of Aging: Age-Related Diseases and Interventions (MIT)

Description

Aging involves an intrinsic and progressive decline in function that eventually will affect us all. While everyone is familiar with aging, many basic questions about aging are mysterious. Why are older people more likely to experience diseases like cancer, stroke, and neurodegenerative disorders? What changes happen at the molecular and cellular levels to cause the changes that we associate with old age? Is aging itself a disease, and can we successfully intervene in the aging process?This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Ad Aging involves an intrinsic and progressive decline in function that eventually will affect us all. While everyone is familiar with aging, many basic questions about aging are mysterious. Why are older people more likely to experience diseases like cancer, stroke, and neurodegenerative disorders? What changes happen at the molecular and cellular levels to cause the changes that we associate with old age? Is aging itself a disease, and can we successfully intervene in the aging process?This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Ad

Subjects

Aging | Aging | age-related diseases | age-related diseases | molecular biology of aging | molecular biology of aging | calorie restriction | calorie restriction | resveratrol | resveratrol | rapamycin | rapamycin | Caloric restriction (CR) | Caloric restriction (CR) | Cellular senescence | Cellular senescence | telomerase | telomerase | progeroid syndromes | progeroid syndromes | mitochondrial DNA | mitochondrial DNA | yeast | yeast | C. elegans | C. elegans | Drosophila | Drosophila | Sirtuins | Sirtuins | SIR4 | SIR4 | target of rapamycin (TOR) | target of rapamycin (TOR) | oxidative damage | oxidative damage | Reactive oxygen species (ROS) | Reactive oxygen species (ROS) | National Institute on Aging Interventions Testing Program | National Institute on Aging Interventions Testing Program | Alzheimer’s disease | Alzheimer’s disease

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases (MIT) 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases (MIT)

Description

The primary role of mitochondria is to produce 90% of a cell's energy in the form of ATP through a process called oxidative phosphorylation. A variety of clinical disorders have been shown to include "mitochondrial dysfunction," which loosely refers to defective oxidative phosphorylation and usually coincides with the occurrence of excess Reactive Oxygen Species (ROS) production, placing cells under oxidative stress. A known cause and effect of oxidative stress is damage to and mutation of mitochondrial DNA. We will use this class to explore issues relating to mitochondrial DNA integrity and how it can be damaged, repaired, mutated, and compromised in human diseases. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These semi The primary role of mitochondria is to produce 90% of a cell's energy in the form of ATP through a process called oxidative phosphorylation. A variety of clinical disorders have been shown to include "mitochondrial dysfunction," which loosely refers to defective oxidative phosphorylation and usually coincides with the occurrence of excess Reactive Oxygen Species (ROS) production, placing cells under oxidative stress. A known cause and effect of oxidative stress is damage to and mutation of mitochondrial DNA. We will use this class to explore issues relating to mitochondrial DNA integrity and how it can be damaged, repaired, mutated, and compromised in human diseases. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These semi

Subjects

mitochondria | mitochondria | human disease | human disease | ATP | ATP | oxidative phosphorylation | oxidative phosphorylation | mitochondrial genome | mitochondrial genome | Reactive Oxygen Species (ROS) | Reactive Oxygen Species (ROS) | mitochondrial dysfunction | mitochondrial dysfunction | oxidative stress | 8-oxoguanine | oxidative stress | 8-oxoguanine | 8-oxoG | 8-oxoG | mtDNA | mtDNA | Ogg1 | Ogg1 | Oxoguanine glycosylase | Oxoguanine glycosylase | mitochondrial DNA polymerase | mitochondrial DNA polymerase | Alzheimer’s disease | Alzheimer’s disease | Parkinson’s disease | Parkinson’s disease | Y955C | Y955C | Mitochondrial DNA depletion syndromes | Mitochondrial DNA depletion syndromes

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.88J Protein Folding and Human Disease (MIT) 7.88J Protein Folding and Human Disease (MIT)

Description

This course covers amino acid sequence control of protein folding, misfolding, amyloid polymerization and aggregation. Readings and discussions address topics such as chaperone structure and function, folding and assembly of fibrous proteins, and pathologies associated with protein misfolding and aggregation in Alzheimer's, Parkinson's, Huntington's and other protein deposition diseases. Students are required to write and present a research paper. This course covers amino acid sequence control of protein folding, misfolding, amyloid polymerization and aggregation. Readings and discussions address topics such as chaperone structure and function, folding and assembly of fibrous proteins, and pathologies associated with protein misfolding and aggregation in Alzheimer's, Parkinson's, Huntington's and other protein deposition diseases. Students are required to write and present a research paper.

Subjects

protein folding | protein folding | misfolding | misfolding | aggregation | aggregation | protein structures | protein structures | folding intermediates | folding intermediates | off-pathway aggregation | off-pathway aggregation | amyloid formation | amyloid formation | Key chaperones | Key chaperones | chaperonins | chaperonins | human protein deposition diseases | human protein deposition diseases | Alzheimer’s disease | Alzheimer’s disease | Parkinson’s disease | Parkinson’s disease | Huntington’s disease | Huntington’s disease | amyloids | amyloids | prions | prions | amino acid sequence | amino acid sequence | amyloid polymerization | amyloid polymerization | chaperone structure and function | chaperone structure and function | folding and assembly of fibrous proteins | folding and assembly of fibrous proteins

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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