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Stanford BIO 118 - Mechanisms of Aging

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Mechanisms of AgingMechanisms of AgingAngela ChenAngela ChenBiochem 118Q: Bioinformatics, Genomics, & MedicineBiochem 118Q: Bioinformatics, Genomics, & MedicineSpring, 2003-2004Spring, 2003-2004AgingAgingTime-related deterioration of theTime-related deterioration of thephysiological functionsphysiological functionsOutlineOutlinennMajor Theories/Hypotheses on AgingMajor Theories/Hypotheses on AgingnnPremature Ageing DiseasesPremature Ageing DiseasesnnWhatWhat’’s in the Future?s in the Future?Major Theories/HypothesesMajor Theories/Hypothesesof Agingof AgingMajor Theories/Hypotheses ofMajor Theories/Hypotheses ofAgingAging1. Reactive Oxygen Species (ROS)1. Reactive Oxygen Species (ROS)2. Genetic Programming of Aging2. Genetic Programming of Aging3. The 3. The ““Wear-and-TearWear-and-Tear”” Theory TheorynnDNA & InformationDNA & InformationnnMitochondriaMitochondriannTelomere & TelomeraseTelomere & Telomerase1. Reactive Oxygen Species1. Reactive Oxygen SpeciesnnNo mutations requiredNo mutations requirednnSenescence = When oxygen atoms inSenescence = When oxygen atoms inthe mitochondria are reduced to ROSthe mitochondria are reduced to ROSnnROSROS = molecules that oxidize and = molecules that oxidize anddamage cell membranes/proteins/damage cell membranes/proteins/nucleic acidsnucleic acidsExamples:Examples:nnP66shc protein in miceP66shc protein in micennCaloric restrictionCaloric restrictionnnVitamins E & CVitamins E & C2. Genetic Programming of Aging2. Genetic Programming of AgingnnHutchinson-Gilford Progeria syndromeHutchinson-Gilford Progeria syndromenn2 examples of 2 examples of C. elegansC. elegans3. 3. ““Wear-and-TearWear-and-Tear”” Theory TheorynnAccumulated point mutationsAccumulated point mutations‡‡SenescenceSenescencennExamples:Examples:nnDNA & InformationDNA & InformationnnMitochondrial mutationsMitochondrial mutationsnnTelomere & TelomeraseTelomere & TelomeraseTelomere & TelomeraseTelomere & Telomerasehttp://www.web-books.com/MoBio/Free/Ch7C.htmHowever, some suggested thatHowever, some suggested that……nnTelomere lengths are independent ofTelomere lengths are independent oflife spanlife spannnThere are no correlations betweenThere are no correlations betweenoneone’’s age and ones age and one’’s telomere lengthss telomere lengthsnnMore research neededMore research neededWho is Geron?Who is Geron?nnBiopharmaceutical company focusing onBiopharmaceutical company focusing ontelomerase, human embryonic stem-cell,telomerase, human embryonic stem-cell,and nuclear transfer researchesand nuclear transfer researchesnnFeb 18Feb 18thth, 2003: , 2003: ““Effects of telomeraseEffects of telomerasetransduction suggest differentialtransduction suggest differentialimpairment of lytic and cytokine functionsimpairment of lytic and cytokine functionsin senescent HIV-1-specific cytotoxic Tin senescent HIV-1-specific cytotoxic Tlymphocyteslymphocytes””Premature Ageing DiseasesPremature Ageing DiseasesPremature Aging DiseasesPremature Aging Diseases1. Down syndrome (Early-onset1. Down syndrome (Early-onset Alzheimer Alzheimer’’s Disease)s Disease)2. Werner2. Werner’’s Syndromes Syndrome3. Hutchinson-Gilford Progeria3. Hutchinson-Gilford Progeria syndrome syndromeDown SyndromeDown Syndrome(Early-onset Alzheimer(Early-onset Alzheimer’’s Disease)s Disease)nnNeurodegenerative disorder: loss ofNeurodegenerative disorder: loss ofmemory, language, & reasoningmemory, language, & reasoningnnAutosomal-dominant genetic diseaseAutosomal-dominant genetic diseaseon chromosome 21on chromosome 21nnEarly onset: 30-40 yearsEarly onset: 30-40 yearsWernerWerner’’s Syndromes SyndromennAutosomal-recessive genetic disease onAutosomal-recessive genetic disease onchromosome 8chromosome 8nnDefective DNA metabolismDefective DNA metabolismnnSymptoms: hair graying/loss, cataracts,Symptoms: hair graying/loss, cataracts,atherosclerosis, osteoporosis (but NOatherosclerosis, osteoporosis (but NOsigns of nuerogeneration, hypertension)signs of nuerogeneration, hypertension)nnAverage living age: 47 yearsAverage living age: 47 yearsHutchinson-Gilford ProgeriaHutchinson-Gilford ProgeriaSyndromeSyndromennSingle dominant mutation on exon 11Single dominant mutation on exon 11of chromosome 1 (Lamin A gene)of chromosome 1 (Lamin A gene)nnSymptoms: dwarfism, arteriosclerosis,Symptoms: dwarfism, arteriosclerosis,myocardial infarctionmyocardial infarctionnnAverage living age: 13.5 yearsAverage living age: 13.5 yearsDatabase ResultsDatabase Results(eMATRIX)(eMATRIX)Lamin ALamin A(Nuclear membrane structure)(Nuclear membrane structure)nnNodavirus coat precursorNodavirus coat precursorendopeptidase (A6)endopeptidase (A6)nnAlpha-2C adrenergicAlpha-2C adrenergicreceptorreceptornnMetabotropic glutamateMetabotropic glutamatereceptor 5receptor 5ProgeriaProgeria[1824 C-T + 1819 [1824 C-T + 1819 –– 1968del] 1968del]nnEB moduleEB modulennClaudin-14Claudin-14Exon 11 only (eMATRIX)Exon 11 only (eMATRIX)ProgeriaProgeriann3.16e-02 3.16e-02 Keratin, high sulfur B2 proteinKeratin, high sulfur B2 protein(3-MTCSITTTAPTAAARGTPLSTTCARAPCCAGPAG-36(3-MTCSITTTAPTAAARGTPLSTTCARAPCCAGPAG-36!!))nn4.54e-01 4.54e-01 Claudin-14 signature IVClaudin-14 signature IV(14-AAARGTPLSTTCA-26)(14-AAARGTPLSTTCA-26)nn7.89e-01 7.89e-01 EB moduleEB module((21-LSTTCARAPCC-31)21-LSTTCARAPCC-31)Lamin ALamin Ann7.14e-02 7.14e-02 Nodavirus coat precursor endopeptidase (A6)Nodavirus coat precursor endopeptidase (A6)aspartic protease signature VIIaspartic protease signature VII ( 69-ATAVWGAVGVAASGT-83)( 69-ATAVWGAVGVAASGT-83)nn8.88e-02 8.88e-02 Keratin, high sulfur B2 proteinKeratin, high sulfur B2 protein((3-MTCSITTTAPTAAARGTPLSTTCARAPCCAGPAG-36)3-MTCSITTTAPTAAARGTPLSTTCARAPCCAGPAG-36)!!nn1.63e-01 1.63e-01 Alpha-2C adrenergic receptor signature IAlpha-2C adrenergic receptor signature I((75-AVGVAASGTIWSPAPTSW-92)75-AVGVAASGTIWSPAPTSW-92)nn9.05e-01 9.05e-01 Metabotropic glutamate receptor 5 sig. VIIMetabotropic glutamate receptor 5 sig. VII(50-RWADPSPLALLP-61)(50-RWADPSPLALLP-61)Telomerase Connections?Telomerase Connections?nnDown syndrome:Down syndrome:Diseased cellDiseased cell’’s telomere length no significants telomere length no significantdifference with normal celldifference with normal cell’’ssnnWernerWerner’’s syndrome:s syndrome:Diseased fibroblastDiseased fibroblast’’s telomere length at senescences telomere length at senescenceslightly longer than


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Stanford BIO 118 - Mechanisms of Aging

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