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You searched for subject:(neurodegeneration). Showing records 1 – 30 of 753 total matches.

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University of Rochester

1. Harder, Jeffrey M. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death.

Degree: PhD, 2013, University of Rochester

 Glaucomas are a group of diseases that often lead to blindness. Glaucomas are unified by the characteristic cell death of the output neuron of the… (more)

Subjects/Keywords: Neurodegeneration

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APA (6th Edition):

Harder, J. M. (2013). The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/26812

Chicago Manual of Style (16th Edition):

Harder, Jeffrey M. “The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death.” 2013. Doctoral Dissertation, University of Rochester. Accessed March 04, 2021. http://hdl.handle.net/1802/26812.

MLA Handbook (7th Edition):

Harder, Jeffrey M. “The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death.” 2013. Web. 04 Mar 2021.

Vancouver:

Harder JM. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1802/26812.

Council of Science Editors:

Harder JM. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/26812


Cornell University

2. Brady, Owen. Investigating Mechanisms Of Ftld-Tdp Pathogenesis.

Degree: PhD, Molecular and Cell Biology, 2014, Cornell University

 Frontotemporal lobar degeneration (FTLD) is a devastating dementia disorder that causes profound changes in personality, behavior, and language abilities. Major breakthroughs in the past decade… (more)

Subjects/Keywords: Neurodegeneration; Lysosomes; TMEM106B

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APA (6th Edition):

Brady, O. (2014). Investigating Mechanisms Of Ftld-Tdp Pathogenesis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36146

Chicago Manual of Style (16th Edition):

Brady, Owen. “Investigating Mechanisms Of Ftld-Tdp Pathogenesis.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36146.

MLA Handbook (7th Edition):

Brady, Owen. “Investigating Mechanisms Of Ftld-Tdp Pathogenesis.” 2014. Web. 04 Mar 2021.

Vancouver:

Brady O. Investigating Mechanisms Of Ftld-Tdp Pathogenesis. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36146.

Council of Science Editors:

Brady O. Investigating Mechanisms Of Ftld-Tdp Pathogenesis. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36146


University of Miami

3. Tseng, LeinWeih Andrew. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2010, University of Miami

  Neuronal pentraxin with chromo domain (NPCD) belongs to a family of neuronally-expressed pentraxin proteins thought to be involved in synaptic refinement and plasticity. One… (more)

Subjects/Keywords: Protein Aggregation; Neurodegeneration

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APA (6th Edition):

Tseng, L. A. (2010). Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/662

Chicago Manual of Style (16th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Doctoral Dissertation, University of Miami. Accessed March 04, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/662.

MLA Handbook (7th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Web. 04 Mar 2021.

Vancouver:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Internet] [Doctoral dissertation]. University of Miami; 2010. [cited 2021 Mar 04]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/662.

Council of Science Editors:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Doctoral Dissertation]. University of Miami; 2010. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/662


University of Miami

4. Tseng, LeinWeih Andrew. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2010, University of Miami

  Neuronal pentraxin with chromo domain (NPCD) belongs to a family of neuronally-expressed pentraxin proteins thought to be involved in synaptic refinement and plasticity. One… (more)

Subjects/Keywords: Protein Aggregation; Neurodegeneration

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APA (6th Edition):

Tseng, L. A. (2010). Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/928

Chicago Manual of Style (16th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Doctoral Dissertation, University of Miami. Accessed March 04, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/928.

MLA Handbook (7th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Web. 04 Mar 2021.

Vancouver:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Internet] [Doctoral dissertation]. University of Miami; 2010. [cited 2021 Mar 04]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/928.

Council of Science Editors:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Doctoral Dissertation]. University of Miami; 2010. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/928


University of Melbourne

5. Welton, Jeremy Morris. Therapeutic implications in genetic prion disease.

Degree: 2011, University of Melbourne

 Prion diseases are fatal neurodegenerative diseases caused by the misfolding of the prion protein (PrP). Of the three subsets of prion diseases (sporadic, genetic, acquired),… (more)

Subjects/Keywords: neurodegeneration; prion; P102L

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APA (6th Edition):

Welton, J. M. (2011). Therapeutic implications in genetic prion disease. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37643

Chicago Manual of Style (16th Edition):

Welton, Jeremy Morris. “Therapeutic implications in genetic prion disease.” 2011. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/37643.

MLA Handbook (7th Edition):

Welton, Jeremy Morris. “Therapeutic implications in genetic prion disease.” 2011. Web. 04 Mar 2021.

Vancouver:

Welton JM. Therapeutic implications in genetic prion disease. [Internet] [Doctoral dissertation]. University of Melbourne; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/37643.

Council of Science Editors:

Welton JM. Therapeutic implications in genetic prion disease. [Doctoral Dissertation]. University of Melbourne; 2011. Available from: http://hdl.handle.net/11343/37643


University of Arizona

6. Coyne, Alyssa N. Dysregulation of mRNA Transport and Translation in ALS .

Degree: 2016, University of Arizona

 Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease affecting upper and lower motor neurons. Although many cellular processes such as cytoskeletal maintenance and synaptic… (more)

Subjects/Keywords: Drosophila; neurodegeneration; ALS

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APA (6th Edition):

Coyne, A. N. (2016). Dysregulation of mRNA Transport and Translation in ALS . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/623181

Chicago Manual of Style (16th Edition):

Coyne, Alyssa N. “Dysregulation of mRNA Transport and Translation in ALS .” 2016. Doctoral Dissertation, University of Arizona. Accessed March 04, 2021. http://hdl.handle.net/10150/623181.

MLA Handbook (7th Edition):

Coyne, Alyssa N. “Dysregulation of mRNA Transport and Translation in ALS .” 2016. Web. 04 Mar 2021.

Vancouver:

Coyne AN. Dysregulation of mRNA Transport and Translation in ALS . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10150/623181.

Council of Science Editors:

Coyne AN. Dysregulation of mRNA Transport and Translation in ALS . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/623181


University of Manchester

7. Howard, Daniel. The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective.

Degree: 2016, University of Manchester

 Alzheimer’s disease (AD) pathogenesis is likely to be caused by dysfunction of two neuronal proteins, amyloid-beta (Aβ) and tau. Whilst excellent in vivo assays have… (more)

Subjects/Keywords: drosophila; neurodegeneration; amyloid; tau

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APA (6th Edition):

Howard, D. (2016). The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556

Chicago Manual of Style (16th Edition):

Howard, Daniel. “The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective.” 2016. Doctoral Dissertation, University of Manchester. Accessed March 04, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556.

MLA Handbook (7th Edition):

Howard, Daniel. “The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective.” 2016. Web. 04 Mar 2021.

Vancouver:

Howard D. The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Mar 04]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556.

Council of Science Editors:

Howard D. The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556


Vanderbilt University

8. Ward, Nicholas John. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Neuronal responses to stress are an important component of neurodegenerative disease and may represent targets for therapeutic intervention. In normal and pathogenic physiological conditions, members… (more)

Subjects/Keywords: neurodegeneration; glaucoma; TRPV1; TRP channels

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APA (6th Edition):

Ward, N. J. (2014). The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13386

Chicago Manual of Style (16th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/13386.

MLA Handbook (7th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Web. 04 Mar 2021.

Vancouver:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/13386.

Council of Science Editors:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/13386


Boston University

9. Bleiberg, Benjamin Aaron. Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila.

Degree: MS, Medical Sciences, 2016, Boston University

 Huntington’s disease (HD) is one of nine polyglutamine diseases and it is caused by a CAG expansion in the HTT gene. HD is an autosomal,… (more)

Subjects/Keywords: Medicine; Drosophila; Neurodegeneration; Huntington's disease

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APA (6th Edition):

Bleiberg, B. A. (2016). Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16770

Chicago Manual of Style (16th Edition):

Bleiberg, Benjamin Aaron. “Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila.” 2016. Masters Thesis, Boston University. Accessed March 04, 2021. http://hdl.handle.net/2144/16770.

MLA Handbook (7th Edition):

Bleiberg, Benjamin Aaron. “Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila.” 2016. Web. 04 Mar 2021.

Vancouver:

Bleiberg BA. Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila. [Internet] [Masters thesis]. Boston University; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2144/16770.

Council of Science Editors:

Bleiberg BA. Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila. [Masters Thesis]. Boston University; 2016. Available from: http://hdl.handle.net/2144/16770


University of Cambridge

10. Sohail, Anood. Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila.

Degree: PhD, 2019, University of Cambridge

 Axons possess a continuous network of smooth tubular endoplasmic reticulum (ER), extending from the nuclear envelope throughout the neuron to synapses. Mutations affecting proteins with… (more)

Subjects/Keywords: Axonal ER; neurodegeneration; drosophila

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APA (6th Edition):

Sohail, A. (2019). Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/290113

Chicago Manual of Style (16th Edition):

Sohail, Anood. “Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/290113.

MLA Handbook (7th Edition):

Sohail, Anood. “Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila.” 2019. Web. 04 Mar 2021.

Vancouver:

Sohail A. Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/290113.

Council of Science Editors:

Sohail A. Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/290113


University of Debrecen

11. Seo, Woo Sung. Role of p53 and PARP-1 in neurodegenerative diseases .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

 The thesis presents a general review of major neurodegenerative diseases and also discusses the role of p53 and PARP-1 in neurodegeneration. p53 and PARP-1 are… (more)

Subjects/Keywords: Neurodegeneration; neuroscience

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APA (6th Edition):

Seo, W. S. (n.d.). Role of p53 and PARP-1 in neurodegenerative diseases . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/243137

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Seo, Woo Sung. “Role of p53 and PARP-1 in neurodegenerative diseases .” Thesis, University of Debrecen. Accessed March 04, 2021. http://hdl.handle.net/2437/243137.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Seo, Woo Sung. “Role of p53 and PARP-1 in neurodegenerative diseases .” Web. 04 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Seo WS. Role of p53 and PARP-1 in neurodegenerative diseases . [Internet] [Thesis]. University of Debrecen; [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2437/243137.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Seo WS. Role of p53 and PARP-1 in neurodegenerative diseases . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/243137

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.


University of Manitoba

12. Acosta, Crystal May R. Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

Degree: Pharmacy, 2013, University of Manitoba

 Nerve growth factor (NGF) represents a new therapeutic strategy for multiple sclerosis (MS) because of its immunomodulatory and neuroprotective activity. To analyze changes in NGF… (more)

Subjects/Keywords: MS; NGF; Neurodegeneration; Neuroimmunology

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APA (6th Edition):

Acosta, C. M. R. (2013). Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/23504

Chicago Manual of Style (16th Edition):

Acosta, Crystal May R. “Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).” 2013. Masters Thesis, University of Manitoba. Accessed March 04, 2021. http://hdl.handle.net/1993/23504.

MLA Handbook (7th Edition):

Acosta, Crystal May R. “Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).” 2013. Web. 04 Mar 2021.

Vancouver:

Acosta CMR. Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). [Internet] [Masters thesis]. University of Manitoba; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1993/23504.

Council of Science Editors:

Acosta CMR. Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). [Masters Thesis]. University of Manitoba; 2013. Available from: http://hdl.handle.net/1993/23504


University of Edinburgh

13. Vincenti, James Edward. Role of activation of microglia in neurodegenerative prion disease.

Degree: PhD, 2015, University of Edinburgh

 Prion diseases are a group of fatal neurodegenerative protein-misfolding diseases. Microglia, the resident myeloid cells found within the brain, have been shown to demonstrate a… (more)

Subjects/Keywords: 612.8; microglia; neurodegeneration; neuroimmunology; prion

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APA (6th Edition):

Vincenti, J. E. (2015). Role of activation of microglia in neurodegenerative prion disease. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/15928

Chicago Manual of Style (16th Edition):

Vincenti, James Edward. “Role of activation of microglia in neurodegenerative prion disease.” 2015. Doctoral Dissertation, University of Edinburgh. Accessed March 04, 2021. http://hdl.handle.net/1842/15928.

MLA Handbook (7th Edition):

Vincenti, James Edward. “Role of activation of microglia in neurodegenerative prion disease.” 2015. Web. 04 Mar 2021.

Vancouver:

Vincenti JE. Role of activation of microglia in neurodegenerative prion disease. [Internet] [Doctoral dissertation]. University of Edinburgh; 2015. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1842/15928.

Council of Science Editors:

Vincenti JE. Role of activation of microglia in neurodegenerative prion disease. [Doctoral Dissertation]. University of Edinburgh; 2015. Available from: http://hdl.handle.net/1842/15928


University of Cambridge

14. Zhu, Ye. Studies on the autophagy gene WIPI4 and its interactor UBR5.

Degree: PhD, 2020, University of Cambridge

 Autophagy is a tightly regulated process that sequesters and delivers proteins and other cellular substances for degradation in the lysosome. Dysfunction of autophagy has been… (more)

Subjects/Keywords: autophagy; proteasome; neurodegeneration disease

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APA (6th Edition):

Zhu, Y. (2020). Studies on the autophagy gene WIPI4 and its interactor UBR5. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/300658

Chicago Manual of Style (16th Edition):

Zhu, Ye. “Studies on the autophagy gene WIPI4 and its interactor UBR5.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/300658.

MLA Handbook (7th Edition):

Zhu, Ye. “Studies on the autophagy gene WIPI4 and its interactor UBR5.” 2020. Web. 04 Mar 2021.

Vancouver:

Zhu Y. Studies on the autophagy gene WIPI4 and its interactor UBR5. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/300658.

Council of Science Editors:

Zhu Y. Studies on the autophagy gene WIPI4 and its interactor UBR5. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/300658


University of Florida

15. Kim, Mi-Jung. Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice.

Degree: PhD, Medical Sciences - Molecular Cell Biology (IDP), 2018, University of Florida

Subjects/Keywords: cochlea; neurodegeneration

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APA (6th Edition):

Kim, M. (2018). Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0051774

Chicago Manual of Style (16th Edition):

Kim, Mi-Jung. “Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice.” 2018. Doctoral Dissertation, University of Florida. Accessed March 04, 2021. https://ufdc.ufl.edu/UFE0051774.

MLA Handbook (7th Edition):

Kim, Mi-Jung. “Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice.” 2018. Web. 04 Mar 2021.

Vancouver:

Kim M. Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice. [Internet] [Doctoral dissertation]. University of Florida; 2018. [cited 2021 Mar 04]. Available from: https://ufdc.ufl.edu/UFE0051774.

Council of Science Editors:

Kim M. Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice. [Doctoral Dissertation]. University of Florida; 2018. Available from: https://ufdc.ufl.edu/UFE0051774


University of Missouri – Columbia

16. Pinnegar, Abbie Jolene. Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia.

Degree: 2012, University of Missouri – Columbia

 [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Unspecified swallowing impairment (dysphagia) was recently reported in dogs with degenerative myelopathy (DM), a… (more)

Subjects/Keywords: dysphagia; brainstem nuclei; neurodegeneration

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APA (6th Edition):

Pinnegar, A. J. (2012). Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/35437

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):

Pinnegar, Abbie Jolene. “Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia.” 2012. Thesis, University of Missouri – Columbia. Accessed March 04, 2021. http://hdl.handle.net/10355/35437.

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

MLA Handbook (7th Edition):

Pinnegar, Abbie Jolene. “Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia.” 2012. Web. 04 Mar 2021.

Vancouver:

Pinnegar AJ. Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia. [Internet] [Thesis]. University of Missouri – Columbia; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10355/35437.

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

Council of Science Editors:

Pinnegar AJ. Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia. [Thesis]. University of Missouri – Columbia; 2012. Available from: http://hdl.handle.net/10355/35437

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


University of Minnesota

17. Amar, Fatou. Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56.

Degree: PhD, Neuroscience, 2016, University of Minnesota

 Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, with asymptomatic and symptomatic phases. Hallmark lesions of AD include extracellular deposits of fibrillar amyloid-β (A β)… (more)

Subjects/Keywords: Alzheimer's disease; molecular neuroscience; neurodegeneration

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APA (6th Edition):

Amar, F. (2016). Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/178973

Chicago Manual of Style (16th Edition):

Amar, Fatou. “Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56.” 2016. Doctoral Dissertation, University of Minnesota. Accessed March 04, 2021. http://hdl.handle.net/11299/178973.

MLA Handbook (7th Edition):

Amar, Fatou. “Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56.” 2016. Web. 04 Mar 2021.

Vancouver:

Amar F. Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56. [Internet] [Doctoral dissertation]. University of Minnesota; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11299/178973.

Council of Science Editors:

Amar F. Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56. [Doctoral Dissertation]. University of Minnesota; 2016. Available from: http://hdl.handle.net/11299/178973


University of Melbourne

18. Price, Katherine Ann. Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration.

Degree: 2012, University of Melbourne

 Alzheimer’s disease (AD) and other neurodegenerative diseases such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are characterized by altered biometal homeostasis. Low intracellular… (more)

Subjects/Keywords: biometals; cell metabolism; trafficking; neurodegeneration

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APA (6th Edition):

Price, K. A. (2012). Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37158

Chicago Manual of Style (16th Edition):

Price, Katherine Ann. “Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration.” 2012. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/37158.

MLA Handbook (7th Edition):

Price, Katherine Ann. “Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration.” 2012. Web. 04 Mar 2021.

Vancouver:

Price KA. Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/37158.

Council of Science Editors:

Price KA. Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37158


University of Melbourne

19. Harrington, Karra. Undetected preclinical neurodegenerative disease in models of normal cognitive aging.

Degree: 2018, University of Melbourne

 With population aging, understanding cognitive changes that occur in late life is vital to support these increasing numbers of older adults to maintain their wellbeing… (more)

Subjects/Keywords: ageing; neurodegeneration; cognition; preclinical Alzheimer

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APA (6th Edition):

Harrington, K. (2018). Undetected preclinical neurodegenerative disease in models of normal cognitive aging. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/219895

Chicago Manual of Style (16th Edition):

Harrington, Karra. “Undetected preclinical neurodegenerative disease in models of normal cognitive aging.” 2018. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/219895.

MLA Handbook (7th Edition):

Harrington, Karra. “Undetected preclinical neurodegenerative disease in models of normal cognitive aging.” 2018. Web. 04 Mar 2021.

Vancouver:

Harrington K. Undetected preclinical neurodegenerative disease in models of normal cognitive aging. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/219895.

Council of Science Editors:

Harrington K. Undetected preclinical neurodegenerative disease in models of normal cognitive aging. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/219895


University of Cambridge

20. Levy, Daniel Robert Siegfried. Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system.

Degree: PhD, 2018, University of Cambridge

 Leucine rich repeat kinase 2 (LRRK2) is a 286 kDa protein expressed in a variety of tissues and cell types, including neuronal tissue and innate… (more)

Subjects/Keywords: 616.8; immunology; Parkinson's disease; neurodegeneration

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APA (6th Edition):

Levy, D. R. S. (2018). Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573

Chicago Manual of Style (16th Edition):

Levy, Daniel Robert Siegfried. “Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system.” 2018. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573.

MLA Handbook (7th Edition):

Levy, Daniel Robert Siegfried. “Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system.” 2018. Web. 04 Mar 2021.

Vancouver:

Levy DRS. Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2021 Mar 04]. Available from: https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573.

Council of Science Editors:

Levy DRS. Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573


University of Sydney

21. Cross, Nathan. Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration .

Degree: 2017, University of Sydney

 There is growing evidence that sleep disturbances share associations with neurodegeneration, and poor sleep is emerging as an independent risk factor for dementia. As a… (more)

Subjects/Keywords: sleep; apnoea; ageing; neurodegeneration

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APA (6th Edition):

Cross, N. (2017). Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17763

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):

Cross, Nathan. “Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration .” 2017. Thesis, University of Sydney. Accessed March 04, 2021. http://hdl.handle.net/2123/17763.

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

MLA Handbook (7th Edition):

Cross, Nathan. “Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration .” 2017. Web. 04 Mar 2021.

Vancouver:

Cross N. Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration . [Internet] [Thesis]. University of Sydney; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2123/17763.

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

Council of Science Editors:

Cross N. Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration . [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/17763

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


University of New South Wales

22. Chiu, Alexander Simon Che-Kean. A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity.

Degree: Biotechnology & Biomolecular Sciences, 2013, University of New South Wales

 The cyanotoxin β-methylamino-L-alanine (BMAA) has long been associated with the elevated incidence of amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC). BMAA has been shown to be… (more)

Subjects/Keywords: ALS/PDC; BMAA; Neurodegeneration; Cyanotoxin

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APA (6th Edition):

Chiu, A. S. C. (2013). A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true

Chicago Manual of Style (16th Edition):

Chiu, Alexander Simon Che-Kean. “A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity.” 2013. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true.

MLA Handbook (7th Edition):

Chiu, Alexander Simon Che-Kean. “A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity.” 2013. Web. 04 Mar 2021.

Vancouver:

Chiu ASC. A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true.

Council of Science Editors:

Chiu ASC. A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true


Texas State University – San Marcos

23. Stavinoha, Rebecca C. In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster.

Degree: MS, Human Nutrition, 2015, Texas State University – San Marcos

No abstract prepared. Advisors/Committee Members: Vattem, Dhiraj A. (advisor), Correia, Roberta (committee member), Apostolidis, Emmanouil (committee member).

Subjects/Keywords: Cinnamon; Neurodegeneration

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APA (6th Edition):

Stavinoha, R. C. (2015). In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster. (Masters Thesis). Texas State University – San Marcos. Retrieved from https://digital.library.txstate.edu/handle/10877/8766

Chicago Manual of Style (16th Edition):

Stavinoha, Rebecca C. “In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster.” 2015. Masters Thesis, Texas State University – San Marcos. Accessed March 04, 2021. https://digital.library.txstate.edu/handle/10877/8766.

MLA Handbook (7th Edition):

Stavinoha, Rebecca C. “In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster.” 2015. Web. 04 Mar 2021.

Vancouver:

Stavinoha RC. In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster. [Internet] [Masters thesis]. Texas State University – San Marcos; 2015. [cited 2021 Mar 04]. Available from: https://digital.library.txstate.edu/handle/10877/8766.

Council of Science Editors:

Stavinoha RC. In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster. [Masters Thesis]. Texas State University – San Marcos; 2015. Available from: https://digital.library.txstate.edu/handle/10877/8766


University of New South Wales

24. Braidy, Nady. NAD+ metabolism in neurodegeneration and aging.

Degree: Medical Sciences, 2011, University of New South Wales

 Elevated levels of several kynurenine pathway (KP) metabolites, e.g. quinolinic acid (QUIN), have been implicated in the aetiology of several neurodegenerative diseases such as Alzheimer‟s… (more)

Subjects/Keywords: NAD+; metabolism; neurodegeneration; aging

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APA (6th Edition):

Braidy, N. (2011). NAD+ metabolism in neurodegeneration and aging. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Braidy, Nady. “NAD+ metabolism in neurodegeneration and aging.” 2011. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true.

MLA Handbook (7th Edition):

Braidy, Nady. “NAD+ metabolism in neurodegeneration and aging.” 2011. Web. 04 Mar 2021.

Vancouver:

Braidy N. NAD+ metabolism in neurodegeneration and aging. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true.

Council of Science Editors:

Braidy N. NAD+ metabolism in neurodegeneration and aging. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true


Rhode Island College

25. DeGrange, Roy W. The Effect of Anesthesia on the Developing Brain.

Degree: MSN, 2019, Rhode Island College

  Damage caused by administering general anesthetics to the developing brain in young children and pregnant mothers is of concern among practicing anesthesia providers. Studies… (more)

Subjects/Keywords:

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APA (6th Edition):

DeGrange, R. W. (2019). The Effect of Anesthesia on the Developing Brain. (Masters Thesis). Rhode Island College. Retrieved from https://digitalcommons.ric.edu/etd/314

Chicago Manual of Style (16th Edition):

DeGrange, Roy W. “The Effect of Anesthesia on the Developing Brain.” 2019. Masters Thesis, Rhode Island College. Accessed March 04, 2021. https://digitalcommons.ric.edu/etd/314.

MLA Handbook (7th Edition):

DeGrange, Roy W. “The Effect of Anesthesia on the Developing Brain.” 2019. Web. 04 Mar 2021.

Vancouver:

DeGrange RW. The Effect of Anesthesia on the Developing Brain. [Internet] [Masters thesis]. Rhode Island College; 2019. [cited 2021 Mar 04]. Available from: https://digitalcommons.ric.edu/etd/314.

Council of Science Editors:

DeGrange RW. The Effect of Anesthesia on the Developing Brain. [Masters Thesis]. Rhode Island College; 2019. Available from: https://digitalcommons.ric.edu/etd/314


University of Cambridge

26. Harris, Kate. Understanding the role of dopamine in pathology and cognition in Huntington’s disease.

Degree: PhD, 2020, University of Cambridge

 Huntington’s disease is a genetic neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin gene. Dysfunction of dopamine (DA) signalling is thought to… (more)

Subjects/Keywords: Neuroscience; Neurodegeneration; Huntington's disease

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APA (6th Edition):

Harris, K. (2020). Understanding the role of dopamine in pathology and cognition in Huntington’s disease. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/315126

Chicago Manual of Style (16th Edition):

Harris, Kate. “Understanding the role of dopamine in pathology and cognition in Huntington’s disease.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/315126.

MLA Handbook (7th Edition):

Harris, Kate. “Understanding the role of dopamine in pathology and cognition in Huntington’s disease.” 2020. Web. 04 Mar 2021.

Vancouver:

Harris K. Understanding the role of dopamine in pathology and cognition in Huntington’s disease. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/315126.

Council of Science Editors:

Harris K. Understanding the role of dopamine in pathology and cognition in Huntington’s disease. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/315126


Kent State University

27. Kumar, Varun. Protein Kinase C Signaling in Neurodegeneration.

Degree: PhD, College of Arts and Sciences / School of Biomedical Sciences, 2016, Kent State University

 Global cerebral ischemia occurs due to cardiac arrest, which results in delayed neurodegeneration. Pharmacological agents such as Protein Kinase C epsilon (PKC epsilon) peptide activators… (more)

Subjects/Keywords: Neurobiology; PKC, Neurodegeneration, ATF2

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APA (6th Edition):

Kumar, V. (2016). Protein Kinase C Signaling in Neurodegeneration. (Doctoral Dissertation). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051

Chicago Manual of Style (16th Edition):

Kumar, Varun. “Protein Kinase C Signaling in Neurodegeneration.” 2016. Doctoral Dissertation, Kent State University. Accessed March 04, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051.

MLA Handbook (7th Edition):

Kumar, Varun. “Protein Kinase C Signaling in Neurodegeneration.” 2016. Web. 04 Mar 2021.

Vancouver:

Kumar V. Protein Kinase C Signaling in Neurodegeneration. [Internet] [Doctoral dissertation]. Kent State University; 2016. [cited 2021 Mar 04]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051.

Council of Science Editors:

Kumar V. Protein Kinase C Signaling in Neurodegeneration. [Doctoral Dissertation]. Kent State University; 2016. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051


University of Cambridge

28. Humoud, Ibrahim. Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration.

Degree: PhD, 2019, University of Cambridge

 Neurodegenerative diseases pose an immense challenge to the population and health care worldwide. There is a growing need for therapeutic strategies to target these diseases.… (more)

Subjects/Keywords: Unfolded Protein Response; Autophagy; Neurodegeneration

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APA (6th Edition):

Humoud, I. (2019). Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/310338

Chicago Manual of Style (16th Edition):

Humoud, Ibrahim. “Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/310338.

MLA Handbook (7th Edition):

Humoud, Ibrahim. “Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration.” 2019. Web. 04 Mar 2021.

Vancouver:

Humoud I. Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/310338.

Council of Science Editors:

Humoud I. Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/310338


University of Alberta

29. Mercer, Robert Corrigan Curtis. The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation.

Degree: PhD, Department of Medicine, 2016, University of Alberta

 Prion diseases are invariably fatal neurodegenerative diseases of humans and other mammals. While they can manifest as sporadic, infectious or genetic etiologies, the central event… (more)

Subjects/Keywords: Gerstmann-Sträussler-Schienker; Potassium Channel; Prion; Neurodegeneration

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APA (6th Edition):

Mercer, R. C. C. (2016). The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/cmp48sc82v

Chicago Manual of Style (16th Edition):

Mercer, Robert Corrigan Curtis. “The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation.” 2016. Doctoral Dissertation, University of Alberta. Accessed March 04, 2021. https://era.library.ualberta.ca/files/cmp48sc82v.

MLA Handbook (7th Edition):

Mercer, Robert Corrigan Curtis. “The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation.” 2016. Web. 04 Mar 2021.

Vancouver:

Mercer RCC. The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation. [Internet] [Doctoral dissertation]. University of Alberta; 2016. [cited 2021 Mar 04]. Available from: https://era.library.ualberta.ca/files/cmp48sc82v.

Council of Science Editors:

Mercer RCC. The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation. [Doctoral Dissertation]. University of Alberta; 2016. Available from: https://era.library.ualberta.ca/files/cmp48sc82v


Vanderbilt University

30. Gibson, Chelsea Lynn. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.

Degree: PhD, Neuroscience, 2018, Vanderbilt University

 Glutamate (Glu) signaling plays a critical role in regulating neural excitability, thus supporting many behaviors. Perturbed Glu homeostasis in the brain is implicated in multiple… (more)

Subjects/Keywords: C. elegans; dopamine; glia; glutamate; excitotoxicity; neurodegeneration

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APA (6th Edition):

Gibson, C. L. (2018). Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11175

Chicago Manual of Style (16th Edition):

Gibson, Chelsea Lynn. “Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/11175.

MLA Handbook (7th Edition):

Gibson, Chelsea Lynn. “Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.” 2018. Web. 04 Mar 2021.

Vancouver:

Gibson CL. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/11175.

Council of Science Editors:

Gibson CL. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/11175

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