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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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7.346 DNA Wars: How the Cell Strikes Back to Avoid Disease after Attacks on DNA (MIT) 7.346 DNA Wars: How the Cell Strikes Back to Avoid Disease after Attacks on DNA (MIT)

Description

A never-ending molecular war takes place in the nucleus of your cells, with DNA damage occurring at a rate of over 20,000 lesions per cell per day. Where does this damage come from, and what are its consequences? What are the differences in the molecular blueprint between individuals who can sustain attacks on DNA and remain healthy compared to those who become sick? 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 Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching. A never-ending molecular war takes place in the nucleus of your cells, with DNA damage occurring at a rate of over 20,000 lesions per cell per day. Where does this damage come from, and what are its consequences? What are the differences in the molecular blueprint between individuals who can sustain attacks on DNA and remain healthy compared to those who become sick? 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 Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.

Subjects

DNA damage | DNA damage | DNA repair | DNA repair | mismatch repair | mismatch repair | direct reversal | direct reversal | nucleotide excision repair | nucleotide excision repair | base excision repair | base excision repair | double strand break repair | double strand break repair | nuclear DNA damage | nuclear DNA damage | mitochondrial DNA damage | mitochondrial DNA damage | Alkylating agents | Alkylating agents | replication errors | replication errors | mutations | mutations | epigenetics | epigenetics | Werner helicase activity | Werner helicase activity

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 Personal Genomics and Medicine: What's in Your Genome? (MIT) 7.342 Personal Genomics and Medicine: What's in Your Genome? (MIT)

Description

Human genome sequencing has revolutionized our understanding of disease susceptibility, drug metabolism and human ancestry. This course will explore how these advances have been made possible by revolutionary new sequencing methodologies that have decreased costs and increased throughput of genome analysis, making it possible to examine genetic correlates for a variety of biological processes and disorders. The course will combine discussions of primary scientific research papers with hands-on data analysis and small group presentations. 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 Human genome sequencing has revolutionized our understanding of disease susceptibility, drug metabolism and human ancestry. This course will explore how these advances have been made possible by revolutionary new sequencing methodologies that have decreased costs and increased throughput of genome analysis, making it possible to examine genetic correlates for a variety of biological processes and disorders. The course will combine discussions of primary scientific research papers with hands-on data analysis and small group presentations. 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

Subjects

genome sequencing | genome sequencing | genome analysis | genome analysis | disease susceptibility | disease susceptibility | drug metabolism | drug metabolism | human ancestry | human ancestry | mitochondrial DNA | mitochondrial DNA | tyrosine kinase inhibitors | tyrosine kinase inhibitors | BCR-ABL gene fusion | BCR-ABL gene fusion | PCSK9 inhibitors | PCSK9 inhibitors | hypercholesterolemia | hypercholesterolemia | genetic testing | genetic testing | next generation sequencing | next generation sequencing | Single-nucleotide polymorphisms (SNPs) | Single-nucleotide polymorphisms (SNPs) | copy number variations (CNVs) | copy number variations (CNVs) | genome-wide association studies (GWAS) | genome-wide association studies (GWAS) | Chronic myelogenous leukemia (CML) | Chronic myelogenous leukemia (CML) | mosaics | mosaics | chimeras | chimeras | bioinformatics | bioinformatics

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 Personal Genomics and Medicine: What's in Your Genome? (MIT)

Description

Human genome sequencing has revolutionized our understanding of disease susceptibility, drug metabolism and human ancestry. This course will explore how these advances have been made possible by revolutionary new sequencing methodologies that have decreased costs and increased throughput of genome analysis, making it possible to examine genetic correlates for a variety of biological processes and disorders. The course will combine discussions of primary scientific research papers with hands-on data analysis and small group presentations. 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

Subjects

genome sequencing | genome analysis | disease susceptibility | drug metabolism | human ancestry | mitochondrial DNA | tyrosine kinase inhibitors | BCR-ABL gene fusion | PCSK9 inhibitors | hypercholesterolemia | genetic testing | next generation sequencing | Single-nucleotide polymorphisms (SNPs) | copy number variations (CNVs) | genome-wide association studies (GWAS) | Chronic myelogenous leukemia (CML) | mosaics | chimeras | bioinformatics

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 https://ocw.mit.edu/terms/index.htm

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7.346 DNA Wars: How the Cell Strikes Back to Avoid Disease after Attacks on DNA (MIT)

Description

A never-ending molecular war takes place in the nucleus of your cells, with DNA damage occurring at a rate of over 20,000 lesions per cell per day. Where does this damage come from, and what are its consequences? What are the differences in the molecular blueprint between individuals who can sustain attacks on DNA and remain healthy compared to those who become sick? 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 Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.

Subjects

DNA damage | DNA repair | mismatch repair | direct reversal | nucleotide excision repair | base excision repair | double strand break repair | nuclear DNA damage | mitochondrial DNA damage | Alkylating agents | replication errors | mutations | epigenetics | Werner helicase activity

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 https://ocw.mit.edu/terms/index.htm

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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

Subjects

Aging | age-related diseases | molecular biology of aging | calorie restriction | resveratrol | rapamycin | Caloric restriction (CR) | Cellular senescence | telomerase | progeroid syndromes | mitochondrial DNA | yeast | C. elegans | Drosophila | Sirtuins | SIR4 | target of rapamycin (TOR) | oxidative damage | Reactive oxygen species (ROS) | National Institute on Aging Interventions Testing Program | ?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 https://ocw.mit.edu/terms/index.htm

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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

Subjects

mitochondria | human disease | ATP | oxidative phosphorylation | mitochondrial genome | Reactive Oxygen Species (ROS) | mitochondrial dysfunction | oxidative stress | 8-oxoguanine | 8-oxoG | mtDNA | Ogg1 | Oxoguanine glycosylase | mitochondrial DNA polymerase | ?s disease | Y955C | 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 https://ocw.mit.edu/terms/index.htm

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