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Prelude no. 2 in A minor, op. 28

ContributorsChopin, Frédéric, 1810-1849 (Composer)

Sonata for cello and piano in G minor, op. 65. III. Largo

ContributorsChopin, Frédéric, 1810-1849 (Composer)
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Generation of a Human Induced Pluripotent Stem Cell Based Model of Progerin Induced Aging

Description
An in vitro model of Alzheimer’s disease (AD) is required to study the poorly understood molecular mechanisms involved in the familial and sporadic forms of the disease. Animal models have previously proven to be useful in studying familial Alzheimer’s disease (AD) by the introduction of AD related mutations in the…

An in vitro model of Alzheimer’s disease (AD) is required to study the poorly understood molecular mechanisms involved in the familial and sporadic forms of the disease. Animal models have previously proven to be useful in studying familial Alzheimer’s disease (AD) by the introduction of AD related mutations in the animal genome and by the overexpression of AD related proteins. The genetics of sporadic Alzheimer’s is however too complex to model in an animal model. More recently, AD human induced pluripotent stem cells (hiPSCs) have been used to study the disease in a dish. However, AD hiPSC derived neurons do not faithfully reflect all the molecular characteristics and phenotypes observed in the aged cells with neurodegenerative disease. The truncated form of nuclear protein Lamin-A, progerin, has been implicated in premature aging and is found in increasing concentrations as normal cells age. We hypothesized that by overexpressing progerin, we can cause cells to ‘age’ and display the neurodegenerative effects observed with aging in both diseased and normal cells. To answer this hypothesis, we first generated a retrovirus that allows for the overexpression of progerin in AD and non-demented control (NDC) hiPSC derived neural progenitor cells(NPCs). Subsequently, we generated a pure population of hNPCs that overexpress progerin and wild type lamin. Finally, we analyzed the presence of various age related phenotypes such as abnormal nuclear structure and the loss of nuclear lamina associated proteins to characterize ‘aging’ in these cells.
ContributorsRaman, Sreedevi (Author) / Brafman, David (Thesis advisor) / Stabenfeldt, Sarah (Committee member) / Wang, Xiao (Committee member) / Arizona State University (Publisher)
Created2017
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Investigation of the Genetic Risk Factors of Alzheimer's Disease and their Physiological Effects

Description

As life expectancy increases worldwide, age related diseases are becoming greater health concerns. One of the most prevalent age-related diseases in the United States is dementia, with Alzheimer’s disease (AD) being the most common form, accounting for 60-80% of cases. Genetics plays a large role in a person’s risk of…

As life expectancy increases worldwide, age related diseases are becoming greater health concerns. One of the most prevalent age-related diseases in the United States is dementia, with Alzheimer’s disease (AD) being the most common form, accounting for 60-80% of cases. Genetics plays a large role in a person’s risk of developing AD. Familial AD, which makes up less than 1% of all AD cases, is caused by autosomal dominant gene mutations and has almost 100% penetrance. Genetic risk factors are believed to make up about 49%-79% of the risk in sporadic cases. Many different genetic risk factors for both familial and sporadic AD have been identified, but there is still much work to be done in the field of AD, especially in non-Caucasian populations. This review summarizes the three major genes responsible for familial AD, namely APP, PSEN1 and PSEN2. Also discussed are seven identified genetic risk factors for sporadic AD, single nucleotide polymorphisms in the APOE, ABCA7, NEDD9, CASS4, PTK2B, CLU, and PICALM genes. An overview of the main function of the proteins associated with the genes is given, along with the supposed connection to AD pathology.
ContributorsRichey, Alexandra Emmeline (Author) / Brafman, David (Thesis director) / Raman, Sreedevi (Committee member) / School of International Letters and Cultures (Contributor) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05

Etude in E major, op. 10 no. 3

ContributorsChopin, Frédéric, 1810-1849 (Composer)

Sonata no. 3 in B minor, op. 58

ContributorsChopin, Frédéric, 1810-1849 (Composer)

Piano sonata no. 3 in B minor, op. 58

ContributorsChopin, Frédéric, 1810-1849 (Composer)

Impromptu no. 3 in G-flat major, op. 51 ; Etude in C-sharp minor, op. 10, no. 4 ; Ballade no. 1 in G minor, op. 23 ; Scherzo no. 1 in B minor, op. 20

ContributorsChopin, Frédéric, 1810-1849 (Composer)

Fantaisie in F minor, op. 49

ContributorsChopin, Frédéric, 1810-1849 (Composer)

Mazurka in C-sharp minor, op. 50, no. 3 ; Nocturne in E major, op. 62, no. 2 ; Ballade in F major, op. 38

ContributorsChopin, Frédéric, 1810-1849 (Composer)