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You searched for subject:(C9ORF72). Showing records 1 – 30 of 32 total matches.

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University of Manchester

1. Hu, Quan. The molecular pathology, genetic involvement and biochemical characteristics of fused in sarcoma (FUS) protein and chromosome 9p-linked frontotemporal lobar degeneration.

Degree: PhD, 2012, University of Manchester

 The fused in sarcoma (FUS) protein has been shown to be a significant disease protein in a subgroup of patients with frontotemporal lobar degeneration (FTLD).… (more)

Subjects/Keywords: 611; FTLD; FUS; C9orf72

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APA (6th Edition):

Hu, Q. (2012). The molecular pathology, genetic involvement and biochemical characteristics of fused in sarcoma (FUS) protein and chromosome 9p-linked frontotemporal lobar degeneration. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-molecular-pathology-genetic-involvement-and-biochemical-characteristics-of-fused-in-sarcoma-fus-protein-and-chromosome-9plinked-frontotemporal-lobar-degeneration(4ac87100-f73a-41c9-a921-f6af5d54dd27).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549104

Chicago Manual of Style (16th Edition):

Hu, Quan. “The molecular pathology, genetic involvement and biochemical characteristics of fused in sarcoma (FUS) protein and chromosome 9p-linked frontotemporal lobar degeneration.” 2012. Doctoral Dissertation, University of Manchester. Accessed July 20, 2019. https://www.research.manchester.ac.uk/portal/en/theses/the-molecular-pathology-genetic-involvement-and-biochemical-characteristics-of-fused-in-sarcoma-fus-protein-and-chromosome-9plinked-frontotemporal-lobar-degeneration(4ac87100-f73a-41c9-a921-f6af5d54dd27).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549104.

MLA Handbook (7th Edition):

Hu, Quan. “The molecular pathology, genetic involvement and biochemical characteristics of fused in sarcoma (FUS) protein and chromosome 9p-linked frontotemporal lobar degeneration.” 2012. Web. 20 Jul 2019.

Vancouver:

Hu Q. The molecular pathology, genetic involvement and biochemical characteristics of fused in sarcoma (FUS) protein and chromosome 9p-linked frontotemporal lobar degeneration. [Internet] [Doctoral dissertation]. University of Manchester; 2012. [cited 2019 Jul 20]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-molecular-pathology-genetic-involvement-and-biochemical-characteristics-of-fused-in-sarcoma-fus-protein-and-chromosome-9plinked-frontotemporal-lobar-degeneration(4ac87100-f73a-41c9-a921-f6af5d54dd27).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549104.

Council of Science Editors:

Hu Q. The molecular pathology, genetic involvement and biochemical characteristics of fused in sarcoma (FUS) protein and chromosome 9p-linked frontotemporal lobar degeneration. [Doctoral Dissertation]. University of Manchester; 2012. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-molecular-pathology-genetic-involvement-and-biochemical-characteristics-of-fused-in-sarcoma-fus-protein-and-chromosome-9plinked-frontotemporal-lobar-degeneration(4ac87100-f73a-41c9-a921-f6af5d54dd27).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549104


University of California – San Diego

2. Pirie, Elaine Christine. Models of TDP-43 Proteinopathy in ALS / FTD and RNA targeting using CRISPR / Cas9.

Degree: Biomedical Sciences, 2017, University of California – San Diego

 Misregulation of RNA processing is a major component of the related neurodegenerative diseases Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration. TDP-43 is an RNA binding protein… (more)

Subjects/Keywords: Neurosciences; Biology; ALS; C9orf72; DM1; DM2; RNA

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APA (6th Edition):

Pirie, E. C. (2017). Models of TDP-43 Proteinopathy in ALS / FTD and RNA targeting using CRISPR / Cas9. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/35k1q39z

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Pirie, Elaine Christine. “Models of TDP-43 Proteinopathy in ALS / FTD and RNA targeting using CRISPR / Cas9.” 2017. Thesis, University of California – San Diego. Accessed July 20, 2019. http://www.escholarship.org/uc/item/35k1q39z.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Pirie, Elaine Christine. “Models of TDP-43 Proteinopathy in ALS / FTD and RNA targeting using CRISPR / Cas9.” 2017. Web. 20 Jul 2019.

Vancouver:

Pirie EC. Models of TDP-43 Proteinopathy in ALS / FTD and RNA targeting using CRISPR / Cas9. [Internet] [Thesis]. University of California – San Diego; 2017. [cited 2019 Jul 20]. Available from: http://www.escholarship.org/uc/item/35k1q39z.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pirie EC. Models of TDP-43 Proteinopathy in ALS / FTD and RNA targeting using CRISPR / Cas9. [Thesis]. University of California – San Diego; 2017. Available from: http://www.escholarship.org/uc/item/35k1q39z

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Tasmania

3. Atkinson, RAK. Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction.

Degree: 2018, University of Tasmania

 A number of proteins have been identified which are pathologically and/or genetically associated with both frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). A hexanucleotide… (more)

Subjects/Keywords: FTD; ALS; TDP-43; C9ORF72; neurite; protein

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APA (6th Edition):

Atkinson, R. (2018). Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/28371/1/Atkinson_whole_thesis.pdf ; https://eprints.utas.edu.au/28371/2/Atkinson%20-%20Thesis%20Appendices.zip ; Atkinson, RAK ORCID: 0000-0002-9846-7738 <https://orcid.org/0000-0002-9846-7738> 2018 , 'Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction', PhD thesis, University of Tasmania.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Atkinson, RAK. “Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction.” 2018. Thesis, University of Tasmania. Accessed July 20, 2019. https://eprints.utas.edu.au/28371/1/Atkinson_whole_thesis.pdf ; https://eprints.utas.edu.au/28371/2/Atkinson%20-%20Thesis%20Appendices.zip ; Atkinson, RAK ORCID: 0000-0002-9846-7738 <https://orcid.org/0000-0002-9846-7738> 2018 , 'Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction', PhD thesis, University of Tasmania..

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Atkinson, RAK. “Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction.” 2018. Web. 20 Jul 2019.

Vancouver:

Atkinson R. Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction. [Internet] [Thesis]. University of Tasmania; 2018. [cited 2019 Jul 20]. Available from: https://eprints.utas.edu.au/28371/1/Atkinson_whole_thesis.pdf ; https://eprints.utas.edu.au/28371/2/Atkinson%20-%20Thesis%20Appendices.zip ; Atkinson, RAK ORCID: 0000-0002-9846-7738 <https://orcid.org/0000-0002-9846-7738> 2018 , 'Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction', PhD thesis, University of Tasmania..

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Atkinson R. Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction. [Thesis]. University of Tasmania; 2018. Available from: https://eprints.utas.edu.au/28371/1/Atkinson_whole_thesis.pdf ; https://eprints.utas.edu.au/28371/2/Atkinson%20-%20Thesis%20Appendices.zip ; Atkinson, RAK ORCID: 0000-0002-9846-7738 <https://orcid.org/0000-0002-9846-7738> 2018 , 'Frontotemporal dementia and amyotrophic lateral sclerosis proteins in neurite health and dysfunction', PhD thesis, University of Tasmania.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Leiden University

4. Herman, Mitch. Gray matter volume in presymptomatic familial frontotemporal dementia.

Degree: 2017, Leiden University

Subjects/Keywords: presymptomatic; FTD; C9ORF72; MAPT; GRN

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APA (6th Edition):

Herman, M. (2017). Gray matter volume in presymptomatic familial frontotemporal dementia. (Masters Thesis). Leiden University. Retrieved from http://hdl.handle.net/1887/51143

Chicago Manual of Style (16th Edition):

Herman, Mitch. “Gray matter volume in presymptomatic familial frontotemporal dementia.” 2017. Masters Thesis, Leiden University. Accessed July 20, 2019. http://hdl.handle.net/1887/51143.

MLA Handbook (7th Edition):

Herman, Mitch. “Gray matter volume in presymptomatic familial frontotemporal dementia.” 2017. Web. 20 Jul 2019.

Vancouver:

Herman M. Gray matter volume in presymptomatic familial frontotemporal dementia. [Internet] [Masters thesis]. Leiden University; 2017. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/1887/51143.

Council of Science Editors:

Herman M. Gray matter volume in presymptomatic familial frontotemporal dementia. [Masters Thesis]. Leiden University; 2017. Available from: http://hdl.handle.net/1887/51143


University of Oxford

5. Scaber, Jakub. The pathophysiological role of TDP-43 in amyotrophic lateral sclerosis due to C9orf72 mutations.

Degree: PhD, 2017, University of Oxford

 Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative condition that affects corticospinal and spinal motor neurons and leads to death within 30 months of symptom onset… (more)

Subjects/Keywords: TDP-43; C9orf72; Motor Neuron Disease; Amyotrophic Lateral Sclerosis

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APA (6th Edition):

Scaber, J. (2017). The pathophysiological role of TDP-43 in amyotrophic lateral sclerosis due to C9orf72 mutations. (Doctoral Dissertation). University of Oxford. Retrieved from https://ora.ox.ac.uk/objects/uuid:c5dd8dcf-c3e0-4ff7-ba9d-bfd3cb9914e8 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.736111

Chicago Manual of Style (16th Edition):

Scaber, Jakub. “The pathophysiological role of TDP-43 in amyotrophic lateral sclerosis due to C9orf72 mutations.” 2017. Doctoral Dissertation, University of Oxford. Accessed July 20, 2019. https://ora.ox.ac.uk/objects/uuid:c5dd8dcf-c3e0-4ff7-ba9d-bfd3cb9914e8 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.736111.

MLA Handbook (7th Edition):

Scaber, Jakub. “The pathophysiological role of TDP-43 in amyotrophic lateral sclerosis due to C9orf72 mutations.” 2017. Web. 20 Jul 2019.

Vancouver:

Scaber J. The pathophysiological role of TDP-43 in amyotrophic lateral sclerosis due to C9orf72 mutations. [Internet] [Doctoral dissertation]. University of Oxford; 2017. [cited 2019 Jul 20]. Available from: https://ora.ox.ac.uk/objects/uuid:c5dd8dcf-c3e0-4ff7-ba9d-bfd3cb9914e8 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.736111.

Council of Science Editors:

Scaber J. The pathophysiological role of TDP-43 in amyotrophic lateral sclerosis due to C9orf72 mutations. [Doctoral Dissertation]. University of Oxford; 2017. Available from: https://ora.ox.ac.uk/objects/uuid:c5dd8dcf-c3e0-4ff7-ba9d-bfd3cb9914e8 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.736111

6. Hu, Quan. The Molecular Pathology, Genetic Involvement and Biochemical Characteristics of Fused in Sarcoma (FUS) Protein and Chromosome 9p-linked Frontotemporal Lobar Degeneration.

Degree: 2012, University of Manchester

 The fused in sarcoma (FUS) protein has been shown to be a significant disease protein in a subgroup of patients with frontotemporal lobar degeneration (FTLD).… (more)

Subjects/Keywords: FTLD; FUS; C9orf72

…187 Table 6.6 Semiquantitative rating of C9orf72 ‘synaptic’ staining in CA sectors with… …Semiquantitative rating of C9orf72 ‘synaptic’ staining in CA sectors with median rating values, for major… …C9orf72 ‘synaptic’ staining in CA sectors between FTLD-TDP subtypes and MND group… …C9orf72 ‘synaptic’ staining in CA sectors between major molecular pathological groups… …208 Table 7.4 Semiquantitative rating of cerebellar p62 pathology and C9orf72 haplotype… 

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APA (6th Edition):

Hu, Q. (2012). The Molecular Pathology, Genetic Involvement and Biochemical Characteristics of Fused in Sarcoma (FUS) Protein and Chromosome 9p-linked Frontotemporal Lobar Degeneration. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:146530

Chicago Manual of Style (16th Edition):

Hu, Quan. “The Molecular Pathology, Genetic Involvement and Biochemical Characteristics of Fused in Sarcoma (FUS) Protein and Chromosome 9p-linked Frontotemporal Lobar Degeneration.” 2012. Doctoral Dissertation, University of Manchester. Accessed July 20, 2019. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:146530.

MLA Handbook (7th Edition):

Hu, Quan. “The Molecular Pathology, Genetic Involvement and Biochemical Characteristics of Fused in Sarcoma (FUS) Protein and Chromosome 9p-linked Frontotemporal Lobar Degeneration.” 2012. Web. 20 Jul 2019.

Vancouver:

Hu Q. The Molecular Pathology, Genetic Involvement and Biochemical Characteristics of Fused in Sarcoma (FUS) Protein and Chromosome 9p-linked Frontotemporal Lobar Degeneration. [Internet] [Doctoral dissertation]. University of Manchester; 2012. [cited 2019 Jul 20]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:146530.

Council of Science Editors:

Hu Q. The Molecular Pathology, Genetic Involvement and Biochemical Characteristics of Fused in Sarcoma (FUS) Protein and Chromosome 9p-linked Frontotemporal Lobar Degeneration. [Doctoral Dissertation]. University of Manchester; 2012. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:146530


University of Edinburgh

7. Cleary, Elaine Marie. Effect of C9orf72 hexanucleotide repeat expansions on human induced pluripotent stem cell derived oligodendrocytes.

Degree: PhD, 2017, University of Edinburgh

 A hexanucleotide repeat expansion in the C9orf72 gene is the most common cause of familial amyotrophic lateral sclerosis and frontotemporal dementia. Genetic testing for this… (more)

Subjects/Keywords: C9orf72 gene; amyotrophic lateral sclerosis; frontotemporal dementia; screening; PCR assays; oligodendrocytes

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APA (6th Edition):

Cleary, E. M. (2017). Effect of C9orf72 hexanucleotide repeat expansions on human induced pluripotent stem cell derived oligodendrocytes. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/28816

Chicago Manual of Style (16th Edition):

Cleary, Elaine Marie. “Effect of C9orf72 hexanucleotide repeat expansions on human induced pluripotent stem cell derived oligodendrocytes.” 2017. Doctoral Dissertation, University of Edinburgh. Accessed July 20, 2019. http://hdl.handle.net/1842/28816.

MLA Handbook (7th Edition):

Cleary, Elaine Marie. “Effect of C9orf72 hexanucleotide repeat expansions on human induced pluripotent stem cell derived oligodendrocytes.” 2017. Web. 20 Jul 2019.

Vancouver:

Cleary EM. Effect of C9orf72 hexanucleotide repeat expansions on human induced pluripotent stem cell derived oligodendrocytes. [Internet] [Doctoral dissertation]. University of Edinburgh; 2017. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/1842/28816.

Council of Science Editors:

Cleary EM. Effect of C9orf72 hexanucleotide repeat expansions on human induced pluripotent stem cell derived oligodendrocytes. [Doctoral Dissertation]. University of Edinburgh; 2017. Available from: http://hdl.handle.net/1842/28816


University of Miami

8. Esanov, Rustam. DNA Hydroxymethylation in Non-coding Repeat Expansion Disorders.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2017, University of Miami

 Hexanucleotide repeat expansion in C9ORF72 gene has recently been shown to cause familial amyotrophic lateral sclerosis, a neurodegenerative disease caused by global death of motor… (more)

Subjects/Keywords: C9ORF72-ALS; Fragile X Syndrome; iPSC; DNA hydroxymethylation; epigenetics

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APA (6th Edition):

Esanov, R. (2017). DNA Hydroxymethylation in Non-coding Repeat Expansion Disorders. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1883

Chicago Manual of Style (16th Edition):

Esanov, Rustam. “DNA Hydroxymethylation in Non-coding Repeat Expansion Disorders.” 2017. Doctoral Dissertation, University of Miami. Accessed July 20, 2019. https://scholarlyrepository.miami.edu/oa_dissertations/1883.

MLA Handbook (7th Edition):

Esanov, Rustam. “DNA Hydroxymethylation in Non-coding Repeat Expansion Disorders.” 2017. Web. 20 Jul 2019.

Vancouver:

Esanov R. DNA Hydroxymethylation in Non-coding Repeat Expansion Disorders. [Internet] [Doctoral dissertation]. University of Miami; 2017. [cited 2019 Jul 20]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1883.

Council of Science Editors:

Esanov R. DNA Hydroxymethylation in Non-coding Repeat Expansion Disorders. [Doctoral Dissertation]. University of Miami; 2017. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1883


University of Arizona

9. Workinger, Paul M. Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia .

Degree: 2017, University of Arizona

 Amyotrophic Lateral Sclerosis (ALS) is a rare and fatal neurodegenerative disorder resulting in the loss of motor neurons from the spinal cord and frontal cortex.… (more)

Subjects/Keywords: ALS; autophagy; C9orf72; intracellular transport; mitochondrial dysfunction; neuronal death

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APA (6th Edition):

Workinger, P. M. (2017). Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia . (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/625350

Chicago Manual of Style (16th Edition):

Workinger, Paul M. “Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia .” 2017. Masters Thesis, University of Arizona. Accessed July 20, 2019. http://hdl.handle.net/10150/625350.

MLA Handbook (7th Edition):

Workinger, Paul M. “Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia .” 2017. Web. 20 Jul 2019.

Vancouver:

Workinger PM. Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia . [Internet] [Masters thesis]. University of Arizona; 2017. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/10150/625350.

Council of Science Editors:

Workinger PM. Familial Amyotrophic Lateral Sclerosis with a focus on C9orf72 Hexanucleotide GGGGCC Repeat Expansion Associated ALS with Frontotemporal Dementia . [Masters Thesis]. University of Arizona; 2017. Available from: http://hdl.handle.net/10150/625350


Cornell University

10. Sullivan, Peter Mayo. Elucidating the disease relevance and function of the ALS/FTLD-associated protein C9orf72 .

Degree: 2017, Cornell University

 Intronic hexanucleotide repeat expansion in the C9orf72 gene is a leading cause of frontotemporal lobar degeneration (FTLD) with amyotrophic lateral sclerosis (ALS). Among several hypotheses,… (more)

Subjects/Keywords: ALS; C9orf72; FTLD; Lysosome; SMCR8; WDR41; Cellular biology; Molecular biology

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APA (6th Edition):

Sullivan, P. M. (2017). Elucidating the disease relevance and function of the ALS/FTLD-associated protein C9orf72 . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/57003

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Sullivan, Peter Mayo. “Elucidating the disease relevance and function of the ALS/FTLD-associated protein C9orf72 .” 2017. Thesis, Cornell University. Accessed July 20, 2019. http://hdl.handle.net/1813/57003.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Sullivan, Peter Mayo. “Elucidating the disease relevance and function of the ALS/FTLD-associated protein C9orf72 .” 2017. Web. 20 Jul 2019.

Vancouver:

Sullivan PM. Elucidating the disease relevance and function of the ALS/FTLD-associated protein C9orf72 . [Internet] [Thesis]. Cornell University; 2017. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/1813/57003.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sullivan PM. Elucidating the disease relevance and function of the ALS/FTLD-associated protein C9orf72 . [Thesis]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/57003

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Erasmus University Rotterdam

11. Riemslagh, Fenne. Molecular Mechanisms of C9ORF72-linked Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Moleculaire mechanismen van C9ORF72 geassocieerde frontotemporale dementie en amyotrofische laterale sclerose.

Degree: Department of Neuroscience, 2019, Erasmus University Rotterdam

 textabstractFrontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are two devastating neurological disorders that share clinical, genetic and pathological overlap. The discovery of a hexanucleotide… (more)

Subjects/Keywords: FTD; ALS; C9ORF72; DPRs

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APA (6th Edition):

Riemslagh, F. (2019). Molecular Mechanisms of C9ORF72-linked Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Moleculaire mechanismen van C9ORF72 geassocieerde frontotemporale dementie en amyotrofische laterale sclerose. (Doctoral Dissertation). Erasmus University Rotterdam. Retrieved from http://hdl.handle.net/1765/117428

Chicago Manual of Style (16th Edition):

Riemslagh, Fenne. “Molecular Mechanisms of C9ORF72-linked Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Moleculaire mechanismen van C9ORF72 geassocieerde frontotemporale dementie en amyotrofische laterale sclerose.” 2019. Doctoral Dissertation, Erasmus University Rotterdam. Accessed July 20, 2019. http://hdl.handle.net/1765/117428.

MLA Handbook (7th Edition):

Riemslagh, Fenne. “Molecular Mechanisms of C9ORF72-linked Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Moleculaire mechanismen van C9ORF72 geassocieerde frontotemporale dementie en amyotrofische laterale sclerose.” 2019. Web. 20 Jul 2019.

Vancouver:

Riemslagh F. Molecular Mechanisms of C9ORF72-linked Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Moleculaire mechanismen van C9ORF72 geassocieerde frontotemporale dementie en amyotrofische laterale sclerose. [Internet] [Doctoral dissertation]. Erasmus University Rotterdam; 2019. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/1765/117428.

Council of Science Editors:

Riemslagh F. Molecular Mechanisms of C9ORF72-linked Frontotemporal Dementia and Amyotrophic Lateral Sclerosis: Moleculaire mechanismen van C9ORF72 geassocieerde frontotemporale dementie en amyotrofische laterale sclerose. [Doctoral Dissertation]. Erasmus University Rotterdam; 2019. Available from: http://hdl.handle.net/1765/117428

12. Lopez-Herdoiza, Maria Belen. Modeling C9ORF72 loss-of-function : a knockdown mouse model : Caractérisation de la perte de fonction de C9ORF72 : un nouveau modèle knockdown.

Degree: Docteur es, Neuroscience, 2016, Université Pierre et Marie Curie – Paris VI

Les démences frontotemporales (DFT) et la sclérose latérale amyotrophique (SLA) sont deux maladies neurodégénératives dévastatrices. La mutation du gène C9ORF72 a été identifiée comme la… (more)

Subjects/Keywords: C9orf72; Sclérose latérale amyotrophique; Démence frontotemporale; Modèle murin; Caractérisation comportementale; Agrégats protéiques; C9orf72 loss of function; Altered autophagy; Amyotrophic lateral sclerosis; 616.8

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APA (6th Edition):

Lopez-Herdoiza, M. B. (2016). Modeling C9ORF72 loss-of-function : a knockdown mouse model : Caractérisation de la perte de fonction de C9ORF72 : un nouveau modèle knockdown. (Doctoral Dissertation). Université Pierre et Marie Curie – Paris VI. Retrieved from http://www.theses.fr/2016PA066239

Chicago Manual of Style (16th Edition):

Lopez-Herdoiza, Maria Belen. “Modeling C9ORF72 loss-of-function : a knockdown mouse model : Caractérisation de la perte de fonction de C9ORF72 : un nouveau modèle knockdown.” 2016. Doctoral Dissertation, Université Pierre et Marie Curie – Paris VI. Accessed July 20, 2019. http://www.theses.fr/2016PA066239.

MLA Handbook (7th Edition):

Lopez-Herdoiza, Maria Belen. “Modeling C9ORF72 loss-of-function : a knockdown mouse model : Caractérisation de la perte de fonction de C9ORF72 : un nouveau modèle knockdown.” 2016. Web. 20 Jul 2019.

Vancouver:

Lopez-Herdoiza MB. Modeling C9ORF72 loss-of-function : a knockdown mouse model : Caractérisation de la perte de fonction de C9ORF72 : un nouveau modèle knockdown. [Internet] [Doctoral dissertation]. Université Pierre et Marie Curie – Paris VI; 2016. [cited 2019 Jul 20]. Available from: http://www.theses.fr/2016PA066239.

Council of Science Editors:

Lopez-Herdoiza MB. Modeling C9ORF72 loss-of-function : a knockdown mouse model : Caractérisation de la perte de fonction de C9ORF72 : un nouveau modèle knockdown. [Doctoral Dissertation]. Université Pierre et Marie Curie – Paris VI; 2016. Available from: http://www.theses.fr/2016PA066239

13. Fourier, Anthony. Vers un marqueur biochimique des dégénérescences lobaires fronto-temporales : variations quantitatives et profils protéiques de la protéine TDP43 dans différentes matrices biologiques : Towards a biochemical marker of fronto temporal lobar degeneration : quantitative variations and qualitative patterns of TDP43 protein in different biological matrices.

Degree: Docteur es, Neurosciences cliniques, 2018, Lyon

Les dégénérescences lobaires frontotemporales (DLFT) représentent la deuxième étiologie neurodégénérative chez l’adulte de moins de 65 ans. Les DLFT sont constituées d’un ensemble hétérogène de… (more)

Subjects/Keywords: Dégénérescence lobaire frontotemporale; Protéinopathies; TDP43; C9ORF72; Profils protéiques; Criblage à haut débit; Biomarqueurs; Frontotemporal lobar degeneration; Proteinopathies; TDP43; C9ORF72; Protein patterns; High throughput screening; Biomarkers; 612.8

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APA (6th Edition):

Fourier, A. (2018). Vers un marqueur biochimique des dégénérescences lobaires fronto-temporales : variations quantitatives et profils protéiques de la protéine TDP43 dans différentes matrices biologiques : Towards a biochemical marker of fronto temporal lobar degeneration : quantitative variations and qualitative patterns of TDP43 protein in different biological matrices. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2018LYSE1269

Chicago Manual of Style (16th Edition):

Fourier, Anthony. “Vers un marqueur biochimique des dégénérescences lobaires fronto-temporales : variations quantitatives et profils protéiques de la protéine TDP43 dans différentes matrices biologiques : Towards a biochemical marker of fronto temporal lobar degeneration : quantitative variations and qualitative patterns of TDP43 protein in different biological matrices.” 2018. Doctoral Dissertation, Lyon. Accessed July 20, 2019. http://www.theses.fr/2018LYSE1269.

MLA Handbook (7th Edition):

Fourier, Anthony. “Vers un marqueur biochimique des dégénérescences lobaires fronto-temporales : variations quantitatives et profils protéiques de la protéine TDP43 dans différentes matrices biologiques : Towards a biochemical marker of fronto temporal lobar degeneration : quantitative variations and qualitative patterns of TDP43 protein in different biological matrices.” 2018. Web. 20 Jul 2019.

Vancouver:

Fourier A. Vers un marqueur biochimique des dégénérescences lobaires fronto-temporales : variations quantitatives et profils protéiques de la protéine TDP43 dans différentes matrices biologiques : Towards a biochemical marker of fronto temporal lobar degeneration : quantitative variations and qualitative patterns of TDP43 protein in different biological matrices. [Internet] [Doctoral dissertation]. Lyon; 2018. [cited 2019 Jul 20]. Available from: http://www.theses.fr/2018LYSE1269.

Council of Science Editors:

Fourier A. Vers un marqueur biochimique des dégénérescences lobaires fronto-temporales : variations quantitatives et profils protéiques de la protéine TDP43 dans différentes matrices biologiques : Towards a biochemical marker of fronto temporal lobar degeneration : quantitative variations and qualitative patterns of TDP43 protein in different biological matrices. [Doctoral Dissertation]. Lyon; 2018. Available from: http://www.theses.fr/2018LYSE1269

14. Erzurumluoğlu, Ebru. Frontotemporal lobar dejenerasyon spektrumunda C9orf72 geni GGGGCC heksanükleotid tekrar artışları ile fenotipik çeşitliliğin karşılaştırılması .

Degree: ESOGÜ, Tıp Fakültesi, Tıbbi Genetik, 2017, Eskisehir Osmangazi University

 Frontotemporal lobar dejenerasyon (FTLD); klinik, patolojik ve genetik olarak heterojen progresif beyin hastalıkları grubunu tanımlamaktadır. Familyal ALS (Amyotrofik lateral skleroz) ve FTD (Frontotemporal Demans)’nin major… (more)

Subjects/Keywords: Frontotemporal Lobar Dejenerasyonu; Frontotemporal Demans; C9orf72; RP-PCR; Sizing-PCR; Frontotemporal Lobar Degeneration; Frontotemporal Dementia

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APA (6th Edition):

Erzurumluoğlu, E. (2017). Frontotemporal lobar dejenerasyon spektrumunda C9orf72 geni GGGGCC heksanükleotid tekrar artışları ile fenotipik çeşitliliğin karşılaştırılması . (Thesis). Eskisehir Osmangazi University. Retrieved from http://hdl.handle.net/11684/1514

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Erzurumluoğlu, Ebru. “Frontotemporal lobar dejenerasyon spektrumunda C9orf72 geni GGGGCC heksanükleotid tekrar artışları ile fenotipik çeşitliliğin karşılaştırılması .” 2017. Thesis, Eskisehir Osmangazi University. Accessed July 20, 2019. http://hdl.handle.net/11684/1514.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Erzurumluoğlu, Ebru. “Frontotemporal lobar dejenerasyon spektrumunda C9orf72 geni GGGGCC heksanükleotid tekrar artışları ile fenotipik çeşitliliğin karşılaştırılması .” 2017. Web. 20 Jul 2019.

Vancouver:

Erzurumluoğlu E. Frontotemporal lobar dejenerasyon spektrumunda C9orf72 geni GGGGCC heksanükleotid tekrar artışları ile fenotipik çeşitliliğin karşılaştırılması . [Internet] [Thesis]. Eskisehir Osmangazi University; 2017. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/11684/1514.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Erzurumluoğlu E. Frontotemporal lobar dejenerasyon spektrumunda C9orf72 geni GGGGCC heksanükleotid tekrar artışları ile fenotipik çeşitliliğin karşılaştırılması . [Thesis]. Eskisehir Osmangazi University; 2017. Available from: http://hdl.handle.net/11684/1514

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Pennsylvania

15. Busch, Johanna Irene. Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways.

Degree: 2016, University of Pennsylvania

 Frontotemporal lobar degeneration (FTLD) is an important cause of dementia in individuals under age 65. Common variants in the TMEM106B gene were previously discovered by… (more)

Subjects/Keywords: C9orf72; Frontotemporal dementia; FTD; FTLD; Lysosome; TMEM106B; Cell Biology; Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Busch, J. I. (2016). Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1630

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Busch, Johanna Irene. “Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways.” 2016. Thesis, University of Pennsylvania. Accessed July 20, 2019. https://repository.upenn.edu/edissertations/1630.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Busch, Johanna Irene. “Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways.” 2016. Web. 20 Jul 2019.

Vancouver:

Busch JI. Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways. [Internet] [Thesis]. University of Pennsylvania; 2016. [cited 2019 Jul 20]. Available from: https://repository.upenn.edu/edissertations/1630.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Busch JI. Increased Expression of Frontotemporal Dementia Risk Factor Tmem106b Alters Lysosomal and Autophagosomal Pathways. [Thesis]. University of Pennsylvania; 2016. Available from: https://repository.upenn.edu/edissertations/1630

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of New South Wales

16. Devenney, Emma. Clinical characteristics and psychiatric features of the C9orf72 expansion.

Degree: Prince of Wales Clinical School, 2016, University of New South Wales

 This thesis aimed to contribute to the literature concerning the clinical characteristics of FTD, and in particular the link between psychosis, psychiatric disorders and the… (more)

Subjects/Keywords: Clinical phenotype; Frontotemporal dementia; Motor neurone disease; C9orf72 genetic expansion; Psychiatric symptoms

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APA (6th Edition):

Devenney, E. (2016). Clinical characteristics and psychiatric features of the C9orf72 expansion. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/59693 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49363/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Devenney, Emma. “Clinical characteristics and psychiatric features of the C9orf72 expansion.” 2016. Doctoral Dissertation, University of New South Wales. Accessed July 20, 2019. http://handle.unsw.edu.au/1959.4/59693 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49363/SOURCE02?view=true.

MLA Handbook (7th Edition):

Devenney, Emma. “Clinical characteristics and psychiatric features of the C9orf72 expansion.” 2016. Web. 20 Jul 2019.

Vancouver:

Devenney E. Clinical characteristics and psychiatric features of the C9orf72 expansion. [Internet] [Doctoral dissertation]. University of New South Wales; 2016. [cited 2019 Jul 20]. Available from: http://handle.unsw.edu.au/1959.4/59693 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49363/SOURCE02?view=true.

Council of Science Editors:

Devenney E. Clinical characteristics and psychiatric features of the C9orf72 expansion. [Doctoral Dissertation]. University of New South Wales; 2016. Available from: http://handle.unsw.edu.au/1959.4/59693 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49363/SOURCE02?view=true

17. Suhonen, N. M. (Noora- Maria). Cognitive and behavioral characteristics of frontotemporal lobar degeneration.

Degree: 2017, University of Oulu

Abstract Frontotemporal lobar degeneration (FTLD) is the second commonest cause of dementia after Alzheimer’s disease (AD) in patients <65 years. Its most frequent clinical subtype… (more)

Subjects/Keywords: behavioral symptoms; dementia; frontotemporal dementia; frontotemporal lobar degeneration; neuropsychological tests; dementia; käytösoireet; neuropsykologia; otsa-ohimolohkorappeumat; otsalohkodementia; C9ORF72

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APA (6th Edition):

Suhonen, N. M. (. M. (2017). Cognitive and behavioral characteristics of frontotemporal lobar degeneration. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789526216102

Chicago Manual of Style (16th Edition):

Suhonen, N M (Noora- Maria). “Cognitive and behavioral characteristics of frontotemporal lobar degeneration.” 2017. Doctoral Dissertation, University of Oulu. Accessed July 20, 2019. http://urn.fi/urn:isbn:9789526216102.

MLA Handbook (7th Edition):

Suhonen, N M (Noora- Maria). “Cognitive and behavioral characteristics of frontotemporal lobar degeneration.” 2017. Web. 20 Jul 2019.

Vancouver:

Suhonen NM(M. Cognitive and behavioral characteristics of frontotemporal lobar degeneration. [Internet] [Doctoral dissertation]. University of Oulu; 2017. [cited 2019 Jul 20]. Available from: http://urn.fi/urn:isbn:9789526216102.

Council of Science Editors:

Suhonen NM(M. Cognitive and behavioral characteristics of frontotemporal lobar degeneration. [Doctoral Dissertation]. University of Oulu; 2017. Available from: http://urn.fi/urn:isbn:9789526216102


Université de Montréal

18. Therrien, Martine. Étude de la toxicité causée par le gène C9orf72 dans la Sclérose Latérale Amyotrophique .

Degree: 2016, Université de Montréal

 La Sclérose Latérale Amyotrophique (SLA) est une maladie neurodégénérative qui affecte les neurones moteurs. 10% des cas sont des cas familiaux et l’étude de ces… (more)

Subjects/Keywords: sclérose latérale amyotrophique; C. elegans; C9orf72; criblage de molecules; dégénérescence; Amyotrophic lateral sclerosis; drug screening; neurodegeneration

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APA (6th Edition):

Therrien, M. (2016). Étude de la toxicité causée par le gène C9orf72 dans la Sclérose Latérale Amyotrophique . (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/16008

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Therrien, Martine. “Étude de la toxicité causée par le gène C9orf72 dans la Sclérose Latérale Amyotrophique .” 2016. Thesis, Université de Montréal. Accessed July 20, 2019. http://hdl.handle.net/1866/16008.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Therrien, Martine. “Étude de la toxicité causée par le gène C9orf72 dans la Sclérose Latérale Amyotrophique .” 2016. Web. 20 Jul 2019.

Vancouver:

Therrien M. Étude de la toxicité causée par le gène C9orf72 dans la Sclérose Latérale Amyotrophique . [Internet] [Thesis]. Université de Montréal; 2016. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/1866/16008.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Therrien M. Étude de la toxicité causée par le gène C9orf72 dans la Sclérose Latérale Amyotrophique . [Thesis]. Université de Montréal; 2016. Available from: http://hdl.handle.net/1866/16008

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


UCLA

19. Swartz, Elliot Wales. Establishment of a human induced pluripotent stem cell derived neuromuscular co-culture system.

Degree: Neuroscience, 2018, UCLA

 Neuromuscular disorders include over 200 rare, monogenic disorders that collectively exceed an incidence of 1 in 3,000 and have few effective treatments. Amyotrophic Lateral Sclerosis… (more)

Subjects/Keywords: Neurosciences; Cellular biology; Amytrophic Lateral Sclerosis; C9orf72; Co-Culture; Induced Pluripotent Stem Cell; Neuromuscular Junction; Optogenetics

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APA (6th Edition):

Swartz, E. W. (2018). Establishment of a human induced pluripotent stem cell derived neuromuscular co-culture system. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/4fx1325n

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Swartz, Elliot Wales. “Establishment of a human induced pluripotent stem cell derived neuromuscular co-culture system.” 2018. Thesis, UCLA. Accessed July 20, 2019. http://www.escholarship.org/uc/item/4fx1325n.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Swartz, Elliot Wales. “Establishment of a human induced pluripotent stem cell derived neuromuscular co-culture system.” 2018. Web. 20 Jul 2019.

Vancouver:

Swartz EW. Establishment of a human induced pluripotent stem cell derived neuromuscular co-culture system. [Internet] [Thesis]. UCLA; 2018. [cited 2019 Jul 20]. Available from: http://www.escholarship.org/uc/item/4fx1325n.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Swartz EW. Establishment of a human induced pluripotent stem cell derived neuromuscular co-culture system. [Thesis]. UCLA; 2018. Available from: http://www.escholarship.org/uc/item/4fx1325n

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Cady, Janet Elizabeth. Genetic Factors that Contribute to the Pathogenesis of Amyotrophic Lateral Sclerosis.

Degree: PhD, Biology & Biomedical Sciences (Human & Statistical Genetics), 2015, Washington University in St. Louis

  Amyotrophic lateral sclerosis (ALS) is fatal neurodegenerative disease for which there is no cure. The only treatment available extends survival by only a matter… (more)

Subjects/Keywords: ALS; C9ORF72; Genetics; Neurodegenerative; Neurogenetics; Sequencing

…List of Figures Figure 1.1 The C9ORF72 gene and its three transcript variants… …75 Figure 4.1: Southern blot confirmation of C9ORF72 repeat expansion in a BAC… …102 Figure 4.2: Largest continuous risk haplotype in patients with full C9ORF72 repeat… …104 Figure 4.3: Largest continuous risk haplotype with intermediate-length C9ORF72 repeat… …110 Figure 5.1: Example of repeat-primed PCR to detect C9ORF72 repeat expansions… 

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APA (6th Edition):

Cady, J. E. (2015). Genetic Factors that Contribute to the Pathogenesis of Amyotrophic Lateral Sclerosis. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/639

Chicago Manual of Style (16th Edition):

Cady, Janet Elizabeth. “Genetic Factors that Contribute to the Pathogenesis of Amyotrophic Lateral Sclerosis.” 2015. Doctoral Dissertation, Washington University in St. Louis. Accessed July 20, 2019. https://openscholarship.wustl.edu/art_sci_etds/639.

MLA Handbook (7th Edition):

Cady, Janet Elizabeth. “Genetic Factors that Contribute to the Pathogenesis of Amyotrophic Lateral Sclerosis.” 2015. Web. 20 Jul 2019.

Vancouver:

Cady JE. Genetic Factors that Contribute to the Pathogenesis of Amyotrophic Lateral Sclerosis. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2015. [cited 2019 Jul 20]. Available from: https://openscholarship.wustl.edu/art_sci_etds/639.

Council of Science Editors:

Cady JE. Genetic Factors that Contribute to the Pathogenesis of Amyotrophic Lateral Sclerosis. [Doctoral Dissertation]. Washington University in St. Louis; 2015. Available from: https://openscholarship.wustl.edu/art_sci_etds/639


Univerzitet u Beogradu

21. Marjanović, Ivan V., 1979-. Kliničko genetska analiza pacijenata sa familijarnom amiotrofičkom lateralnom sklerozom u populaciji Srbije.

Degree: Medicinski fakultet, 2019, Univerzitet u Beogradu

medicina - neurologija / medicine - neurology

Amiotrofična lateralna skleroza (ALS) nastaje usled primarnog oštećenja motornih neurona na nivou kore velikog mozga, jedara moždanog stabla… (more)

Subjects/Keywords: lateral sclerosis (ALS); SOD1 gene; c9orf72; cognition; diffusion tensor imaging; cortical thickness; functional brain MRI; spinal cord atrophy

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APA (6th Edition):

Marjanović, Ivan V., 1. (2019). Kliničko genetska analiza pacijenata sa familijarnom amiotrofičkom lateralnom sklerozom u populaciji Srbije. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:19410/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Marjanović, Ivan V., 1979-. “Kliničko genetska analiza pacijenata sa familijarnom amiotrofičkom lateralnom sklerozom u populaciji Srbije.” 2019. Thesis, Univerzitet u Beogradu. Accessed July 20, 2019. https://fedorabg.bg.ac.rs/fedora/get/o:19410/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Marjanović, Ivan V., 1979-. “Kliničko genetska analiza pacijenata sa familijarnom amiotrofičkom lateralnom sklerozom u populaciji Srbije.” 2019. Web. 20 Jul 2019.

Vancouver:

Marjanović, Ivan V. 1. Kliničko genetska analiza pacijenata sa familijarnom amiotrofičkom lateralnom sklerozom u populaciji Srbije. [Internet] [Thesis]. Univerzitet u Beogradu; 2019. [cited 2019 Jul 20]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19410/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Marjanović, Ivan V. 1. Kliničko genetska analiza pacijenata sa familijarnom amiotrofičkom lateralnom sklerozom u populaciji Srbije. [Thesis]. Univerzitet u Beogradu; 2019. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19410/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Pennsylvania

22. Liu, Elaine. Molecular Analysis Of Amyotrophic Lateral Sclerosis And Frontotemporal Degeneration Brain Tissue Identifies Disease Mechanisms Associated With Repetitive Dna Elements.

Degree: 2017, University of Pennsylvania

 Aging-related neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) are two fatal progressive neurodegenerative diseases that carry genetic and pathologic overlap:… (more)

Subjects/Keywords: ALS/FTD; C9orf72; methylation; neurodegeneration; RNA binding proteins; TDP-43; Molecular Biology; Neuroscience and Neurobiology; Pathology

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APA (6th Edition):

Liu, E. (2017). Molecular Analysis Of Amyotrophic Lateral Sclerosis And Frontotemporal Degeneration Brain Tissue Identifies Disease Mechanisms Associated With Repetitive Dna Elements. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/2697

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Liu, Elaine. “Molecular Analysis Of Amyotrophic Lateral Sclerosis And Frontotemporal Degeneration Brain Tissue Identifies Disease Mechanisms Associated With Repetitive Dna Elements.” 2017. Thesis, University of Pennsylvania. Accessed July 20, 2019. https://repository.upenn.edu/edissertations/2697.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Liu, Elaine. “Molecular Analysis Of Amyotrophic Lateral Sclerosis And Frontotemporal Degeneration Brain Tissue Identifies Disease Mechanisms Associated With Repetitive Dna Elements.” 2017. Web. 20 Jul 2019.

Vancouver:

Liu E. Molecular Analysis Of Amyotrophic Lateral Sclerosis And Frontotemporal Degeneration Brain Tissue Identifies Disease Mechanisms Associated With Repetitive Dna Elements. [Internet] [Thesis]. University of Pennsylvania; 2017. [cited 2019 Jul 20]. Available from: https://repository.upenn.edu/edissertations/2697.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Liu E. Molecular Analysis Of Amyotrophic Lateral Sclerosis And Frontotemporal Degeneration Brain Tissue Identifies Disease Mechanisms Associated With Repetitive Dna Elements. [Thesis]. University of Pennsylvania; 2017. Available from: https://repository.upenn.edu/edissertations/2697

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Oulu

23. Rytty, R. (Riikka). Resting-state functional MRI in behavioral variant of frontotemporal dementia.

Degree: 2016, University of Oulu

Abstract Frontotemporal lobar degeneration (FTLD) is the second most common neurodegenerative disease leading to early-onset dementia with an estimated worldwide prevalence of 10 to 30… (more)

Subjects/Keywords: behavioral variant frontotemporal dementia; default mode network; functional MRI; resting-state; salience network; lepotila; olennaisen tunnistava hermoverkko; otsalohkodementia; toiminnallinen magneettikuvaus; valve-lepotilan hermoverkko; C9ORF72

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APA (6th Edition):

Rytty, R. (. (2016). Resting-state functional MRI in behavioral variant of frontotemporal dementia. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789526211336

Chicago Manual of Style (16th Edition):

Rytty, R (Riikka). “Resting-state functional MRI in behavioral variant of frontotemporal dementia.” 2016. Doctoral Dissertation, University of Oulu. Accessed July 20, 2019. http://urn.fi/urn:isbn:9789526211336.

MLA Handbook (7th Edition):

Rytty, R (Riikka). “Resting-state functional MRI in behavioral variant of frontotemporal dementia.” 2016. Web. 20 Jul 2019.

Vancouver:

Rytty R(. Resting-state functional MRI in behavioral variant of frontotemporal dementia. [Internet] [Doctoral dissertation]. University of Oulu; 2016. [cited 2019 Jul 20]. Available from: http://urn.fi/urn:isbn:9789526211336.

Council of Science Editors:

Rytty R(. Resting-state functional MRI in behavioral variant of frontotemporal dementia. [Doctoral Dissertation]. University of Oulu; 2016. Available from: http://urn.fi/urn:isbn:9789526211336


Universitat Pompeu Fabra

24. Dols Icardo, Oriol, 1987-. Assessing the genetic overlap in amyotrophic lateral sclerosis and frontotemporal dementia.

Degree: Departament de Ciències Experimentals i de la Salut, 2016, Universitat Pompeu Fabra

 Una gran quantitat d’evidències suggereixen que l’esclerosi lateral amiotròfica (ELA) i la demència frontotemporal (DFT) formen part d’un contínuum clínic, patològic i genètic. L’expansió d’un… (more)

Subjects/Keywords: Amyotrophic lateral sclerosis; Frontotemporal dementia; Genetic overlap; C9orf72; Whole-exome sequencing; Esclerosi lateral amiotròfica; Demència frontotemporal; Solapament genètic; Seqüenciació de l’exoma; 575

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Dols Icardo, Oriol, 1. (2016). Assessing the genetic overlap in amyotrophic lateral sclerosis and frontotemporal dementia. (Thesis). Universitat Pompeu Fabra. Retrieved from http://hdl.handle.net/10803/523545

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Dols Icardo, Oriol, 1987-. “Assessing the genetic overlap in amyotrophic lateral sclerosis and frontotemporal dementia.” 2016. Thesis, Universitat Pompeu Fabra. Accessed July 20, 2019. http://hdl.handle.net/10803/523545.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Dols Icardo, Oriol, 1987-. “Assessing the genetic overlap in amyotrophic lateral sclerosis and frontotemporal dementia.” 2016. Web. 20 Jul 2019.

Vancouver:

Dols Icardo, Oriol 1. Assessing the genetic overlap in amyotrophic lateral sclerosis and frontotemporal dementia. [Internet] [Thesis]. Universitat Pompeu Fabra; 2016. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/10803/523545.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dols Icardo, Oriol 1. Assessing the genetic overlap in amyotrophic lateral sclerosis and frontotemporal dementia. [Thesis]. Universitat Pompeu Fabra; 2016. Available from: http://hdl.handle.net/10803/523545

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


The Ohio State University

25. Klepek, Holly N. Genetic testing in Amyotrophic Lateral Sclerosis: A Survey of ALS Clinicians and Commercial Testing Laboratories.

Degree: MS, Genetic Counseling, 2018, The Ohio State University

 Background: Although there is an increase of clinicians offering ALS genetic testing, the practice of offering genetic testing in the management of patients with ALS… (more)

Subjects/Keywords: Genetics; Biology; Health Care; Health Care Management; Medicine; Neurology; Amyotrophic Lateral Sclerosis; ALS; Clinician Attitude; ALS Laboratory; C9orf72; SOD1; ALS Commercial Genetic Testing; Genetic Counseling

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APA (6th Edition):

Klepek, H. N. (2018). Genetic testing in Amyotrophic Lateral Sclerosis: A Survey of ALS Clinicians and Commercial Testing Laboratories. (Masters Thesis). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1523829253204339

Chicago Manual of Style (16th Edition):

Klepek, Holly N. “Genetic testing in Amyotrophic Lateral Sclerosis: A Survey of ALS Clinicians and Commercial Testing Laboratories.” 2018. Masters Thesis, The Ohio State University. Accessed July 20, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523829253204339.

MLA Handbook (7th Edition):

Klepek, Holly N. “Genetic testing in Amyotrophic Lateral Sclerosis: A Survey of ALS Clinicians and Commercial Testing Laboratories.” 2018. Web. 20 Jul 2019.

Vancouver:

Klepek HN. Genetic testing in Amyotrophic Lateral Sclerosis: A Survey of ALS Clinicians and Commercial Testing Laboratories. [Internet] [Masters thesis]. The Ohio State University; 2018. [cited 2019 Jul 20]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1523829253204339.

Council of Science Editors:

Klepek HN. Genetic testing in Amyotrophic Lateral Sclerosis: A Survey of ALS Clinicians and Commercial Testing Laboratories. [Masters Thesis]. The Ohio State University; 2018. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1523829253204339


University of Oulu

26. Kaivorinne, A.-L. (Anna-Lotta). Frontotemporal lobar degeneration in Finland:molecular genetics and clinical aspects.

Degree: 2012, University of Oulu

Abstract Frontotemporal lobar degeneration (FTLD) is the second most common neurodegenerative disease leading to early-onset dementia (< 65 years), next to Alzheimer’s disease. FTLD is substantially… (more)

Subjects/Keywords: C9ORF72; TAR DNA binding protein; charged multi-vesicular body protein 2B; dementia; frontotemporal dementia; frontotemporal lobar degeneration; genetics; haplotype; microtubule-associated protein tau; molecular genetics; mutation; phenotype; polymorphism; repeat expansion; dementia; geenit; geneettinen assosiaatioanalyysi; genetiikka; genotyyppi; molekyyligenetiikka; mutaatiot; otsa-ohimolohkorappeumat

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Kaivorinne, A. -. (. (2012). Frontotemporal lobar degeneration in Finland:molecular genetics and clinical aspects. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789526200132

Chicago Manual of Style (16th Edition):

Kaivorinne, A -L (Anna-Lotta). “Frontotemporal lobar degeneration in Finland:molecular genetics and clinical aspects.” 2012. Doctoral Dissertation, University of Oulu. Accessed July 20, 2019. http://urn.fi/urn:isbn:9789526200132.

MLA Handbook (7th Edition):

Kaivorinne, A -L (Anna-Lotta). “Frontotemporal lobar degeneration in Finland:molecular genetics and clinical aspects.” 2012. Web. 20 Jul 2019.

Vancouver:

Kaivorinne A-(. Frontotemporal lobar degeneration in Finland:molecular genetics and clinical aspects. [Internet] [Doctoral dissertation]. University of Oulu; 2012. [cited 2019 Jul 20]. Available from: http://urn.fi/urn:isbn:9789526200132.

Council of Science Editors:

Kaivorinne A-(. Frontotemporal lobar degeneration in Finland:molecular genetics and clinical aspects. [Doctoral Dissertation]. University of Oulu; 2012. Available from: http://urn.fi/urn:isbn:9789526200132


University of Oxford

27. Douglas, Andrew Graham Lim. Oligonucleotide-based therapies for neuromuscular disease.

Degree: PhD, 2015, University of Oxford

 Genetic neuromuscular diseases remain essentially untreatable. Duchenne muscular dystrophy (DMD) is one such example and another is C9ORF72-related frontotemporal dementia/amyotrophic lateral sclerosis (c9FTD/ALS). Both these… (more)

Subjects/Keywords: 616.7; Medical Sciences; Gene medicine; Genetics (medical sciences); Neuroscience; Motor neurone degenerative disease; Muscle & Nerve (Neuroscience); Clinical genetics; Ultrastructural morphology; Pharmacology; Duchenne muscular dystrophy; mdx; motor neuron disease; amyotrophic lateral sclerosis; fronto-temporal dementia; C9orf72; c9FTD/ALS; antisense oligonucleotides; blood-brain barrier

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Douglas, A. G. L. (2015). Oligonucleotide-based therapies for neuromuscular disease. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:d14706a3-c436-46ff-87c4-40bbbad6dc01 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664806

Chicago Manual of Style (16th Edition):

Douglas, Andrew Graham Lim. “Oligonucleotide-based therapies for neuromuscular disease.” 2015. Doctoral Dissertation, University of Oxford. Accessed July 20, 2019. http://ora.ox.ac.uk/objects/uuid:d14706a3-c436-46ff-87c4-40bbbad6dc01 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664806.

MLA Handbook (7th Edition):

Douglas, Andrew Graham Lim. “Oligonucleotide-based therapies for neuromuscular disease.” 2015. Web. 20 Jul 2019.

Vancouver:

Douglas AGL. Oligonucleotide-based therapies for neuromuscular disease. [Internet] [Doctoral dissertation]. University of Oxford; 2015. [cited 2019 Jul 20]. Available from: http://ora.ox.ac.uk/objects/uuid:d14706a3-c436-46ff-87c4-40bbbad6dc01 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664806.

Council of Science Editors:

Douglas AGL. Oligonucleotide-based therapies for neuromuscular disease. [Doctoral Dissertation]. University of Oxford; 2015. Available from: http://ora.ox.ac.uk/objects/uuid:d14706a3-c436-46ff-87c4-40bbbad6dc01 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664806

28. Cohn-Hokke, PE. Hereditary dementia, a clinical genetic perspective.

Degree: 2017, NARCIS

Subjects/Keywords: dementia; Alzheimer's disease; frontotemporal dementia; genetics; APOE; SORL1; C9orf72; genotype; phenotype; mutation; genetic counselling; hereditary

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Cohn-Hokke, P. (2017). Hereditary dementia, a clinical genetic perspective. (Doctoral Dissertation). NARCIS. Retrieved from https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; 3a31420a-13d8-4d86-ac98-52de32e148df ; 1871/55205 ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df

Chicago Manual of Style (16th Edition):

Cohn-Hokke, PE. “Hereditary dementia, a clinical genetic perspective.” 2017. Doctoral Dissertation, NARCIS. Accessed July 20, 2019. https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; 3a31420a-13d8-4d86-ac98-52de32e148df ; 1871/55205 ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df.

MLA Handbook (7th Edition):

Cohn-Hokke, PE. “Hereditary dementia, a clinical genetic perspective.” 2017. Web. 20 Jul 2019.

Vancouver:

Cohn-Hokke P. Hereditary dementia, a clinical genetic perspective. [Internet] [Doctoral dissertation]. NARCIS; 2017. [cited 2019 Jul 20]. Available from: https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; 3a31420a-13d8-4d86-ac98-52de32e148df ; 1871/55205 ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df.

Council of Science Editors:

Cohn-Hokke P. Hereditary dementia, a clinical genetic perspective. [Doctoral Dissertation]. NARCIS; 2017. Available from: https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; 3a31420a-13d8-4d86-ac98-52de32e148df ; 1871/55205 ; urn:nbn:nl:ui:31-3a31420a-13d8-4d86-ac98-52de32e148df ; https://research.vumc.nl/en/publications/3a31420a-13d8-4d86-ac98-52de32e148df


Vrije Universiteit Amsterdam

29. Cohn-Hokke, P.E. Hereditary dementia, a clinical genetic perspective .

Degree: 2017, Vrije Universiteit Amsterdam

Subjects/Keywords: dementia; Alzheimer's disease; frontotemporal dementia; genetics; APOE; SORL1; C9orf72; genotype; phenotype; mutation; genetic counselling; hereditary

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Cohn-Hokke, P. E. (2017). Hereditary dementia, a clinical genetic perspective . (Doctoral Dissertation). Vrije Universiteit Amsterdam. Retrieved from http://hdl.handle.net/1871/55205

Chicago Manual of Style (16th Edition):

Cohn-Hokke, P E. “Hereditary dementia, a clinical genetic perspective .” 2017. Doctoral Dissertation, Vrije Universiteit Amsterdam. Accessed July 20, 2019. http://hdl.handle.net/1871/55205.

MLA Handbook (7th Edition):

Cohn-Hokke, P E. “Hereditary dementia, a clinical genetic perspective .” 2017. Web. 20 Jul 2019.

Vancouver:

Cohn-Hokke PE. Hereditary dementia, a clinical genetic perspective . [Internet] [Doctoral dissertation]. Vrije Universiteit Amsterdam; 2017. [cited 2019 Jul 20]. Available from: http://hdl.handle.net/1871/55205.

Council of Science Editors:

Cohn-Hokke PE. Hereditary dementia, a clinical genetic perspective . [Doctoral Dissertation]. Vrije Universiteit Amsterdam; 2017. Available from: http://hdl.handle.net/1871/55205


University of New South Wales

30. Loy, Clement Tien-Hui. Clinical & molecular genetics of frontotemporal dementia.

Degree: Clinical School - St Vincent's Hospital, 2013, University of New South Wales

 Frontotemporal Dementia (FTD) is a heterogeneous group of disorders, characterised byprogressive degeneration of the frontal/temporal lobes. Up to 30% of people with FTDhave an autosomal… (more)

Subjects/Keywords: Clinical genetics; Molecular genetics; Frontotemporal dementia (FTD); Frontal/temporal lobes; Motor Neuron Disease (MND); C9ORF72; Autosomal dominant family history; Microtubule-associated protein Tau (MAPT); MAPT haplotype; Glycogen Synthase Kinase-3B (GSK3B); Alzheimer Disease; Parkinson Disease; Progranulin (GRN); GRN mutation (Q300X)

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APA (6th Edition):

Loy, C. T. (2013). Clinical & molecular genetics of frontotemporal dementia. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53844 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12531/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Loy, Clement Tien-Hui. “Clinical & molecular genetics of frontotemporal dementia.” 2013. Doctoral Dissertation, University of New South Wales. Accessed July 20, 2019. http://handle.unsw.edu.au/1959.4/53844 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12531/SOURCE02?view=true.

MLA Handbook (7th Edition):

Loy, Clement Tien-Hui. “Clinical & molecular genetics of frontotemporal dementia.” 2013. Web. 20 Jul 2019.

Vancouver:

Loy CT. Clinical & molecular genetics of frontotemporal dementia. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2019 Jul 20]. Available from: http://handle.unsw.edu.au/1959.4/53844 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12531/SOURCE02?view=true.

Council of Science Editors:

Loy CT. Clinical & molecular genetics of frontotemporal dementia. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/53844 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12531/SOURCE02?view=true

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