Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

Country:

You searched for subject:(neurodegeneration). Showing records 1 – 30 of 250 total matches.

[1] [2] [3] [4] [5] [6] [7] [8] [9]

Search Limiters

Last 2 Years | English Only

Department

Degrees

Levels

▼ Search Limiters


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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. 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. 18 Aug 2019.

Vancouver:

Harder JM. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2019 Aug 18]. 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: 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

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

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):

Brady, Owen. “Investigating Mechanisms Of Ftld-Tdp Pathogenesis .” 2014. Thesis, Cornell University. Accessed August 18, 2019. http://hdl.handle.net/1813/36146.

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

MLA Handbook (7th Edition):

Brady, Owen. “Investigating Mechanisms Of Ftld-Tdp Pathogenesis .” 2014. Web. 18 Aug 2019.

Vancouver:

Brady O. Investigating Mechanisms Of Ftld-Tdp Pathogenesis . [Internet] [Thesis]. Cornell University; 2014. [cited 2019 Aug 18]. Available from: http://hdl.handle.net/1813/36146.

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

Council of Science Editors:

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

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


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 isoform… (more)

Subjects/Keywords: Protein Aggregation; Neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. 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. 18 Aug 2019.

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 2019 Aug 18]. 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 isoform… (more)

Subjects/Keywords: Protein Aggregation; Neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. 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. 18 Aug 2019.

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 2019 Aug 18]. 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 Arizona

5. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. http://hdl.handle.net/10150/623181.

MLA Handbook (7th Edition):

Coyne, Alyssa N. “Dysregulation of mRNA Transport and Translation in ALS .” 2016. Web. 18 Aug 2019.

Vancouver:

Coyne AN. Dysregulation of mRNA Transport and Translation in ALS . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2019 Aug 18]. 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


Kent State University

6. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051.

MLA Handbook (7th Edition):

Kumar, Varun. “Protein Kinase C Signaling in Neurodegeneration.” 2016. Web. 18 Aug 2019.

Vancouver:

Kumar V. Protein Kinase C Signaling in Neurodegeneration. [Internet] [Doctoral dissertation]. Kent State University; 2016. [cited 2019 Aug 18]. 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


Vanderbilt University

7. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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://etd.library.vanderbilt.edu/available/etd-07212014-152449/ ;

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 August 18, 2019. http://etd.library.vanderbilt.edu/available/etd-07212014-152449/ ;.

MLA Handbook (7th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Web. 18 Aug 2019.

Vancouver:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Aug 18]. Available from: http://etd.library.vanderbilt.edu/available/etd-07212014-152449/ ;.

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://etd.library.vanderbilt.edu/available/etd-07212014-152449/ ;


University of Minnesota

8. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. 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. 18 Aug 2019.

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 2019 Aug 18]. 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 Pennsylvania

9. Covy, Jason P. The Pathological and Biochemical Characterization of Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease.

Degree: 2010, University of Pennsylvania

 Parkinson's disease (PD) is a debilitating and progressive neurodegenerative disorder that affects over 6 million people worldwide. Despite being the most common movement disorder in… (more)

Subjects/Keywords: LRRK2; Parkinson's disease; neurodegeneration; Neurosciences

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Covy, J. P. (2010). The Pathological and Biochemical Characterization of Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1553

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):

Covy, Jason P. “The Pathological and Biochemical Characterization of Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease.” 2010. Thesis, University of Pennsylvania. Accessed August 18, 2019. https://repository.upenn.edu/edissertations/1553.

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

MLA Handbook (7th Edition):

Covy, Jason P. “The Pathological and Biochemical Characterization of Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease.” 2010. Web. 18 Aug 2019.

Vancouver:

Covy JP. The Pathological and Biochemical Characterization of Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease. [Internet] [Thesis]. University of Pennsylvania; 2010. [cited 2019 Aug 18]. Available from: https://repository.upenn.edu/edissertations/1553.

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

Council of Science Editors:

Covy JP. The Pathological and Biochemical Characterization of Leucine-Rich Repeat Kinase 2 in Parkinson’s Disease. [Thesis]. University of Pennsylvania; 2010. Available from: https://repository.upenn.edu/edissertations/1553

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


University of Missouri – Columbia

10. 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 AUTHOR'S REQUEST.] Unspecified swallowing impairment (dysphagia) was recently reported in dogs with degenerative myelopathy (DM), a proposed… (more)

Subjects/Keywords: dysphagia; brainstem nuclei; neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. 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. 18 Aug 2019.

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 2019 Aug 18]. 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


Boston University

11. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 August 18, 2019. 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. 18 Aug 2019.

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 2019 Aug 18]. 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


Texas A&M University

12. Huang, Pei-San. Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain.

Degree: 2012, Texas A&M University

 Nicotine, the major psychoactive ingredient of tobacco smoke, underlies numerous effects by activating neuronal nicotinic acetylcholine receptors. Both in vitro and in vivo studies suggest… (more)

Subjects/Keywords: nicotine; neuroprotection; aging; nAChRs; neurodegeneration; caloric restriction

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Huang, P. (2012). Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067

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):

Huang, Pei-San. “Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain.” 2012. Thesis, Texas A&M University. Accessed August 18, 2019. http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067.

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

MLA Handbook (7th Edition):

Huang, Pei-San. “Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain.” 2012. Web. 18 Aug 2019.

Vancouver:

Huang P. Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain. [Internet] [Thesis]. Texas A&M University; 2012. [cited 2019 Aug 18]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067.

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

Council of Science Editors:

Huang P. Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain. [Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067

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


Wright State University

13. Davidson, Molly Elizabeth. Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin Exposure.

Degree: MS, Pharmacology and Toxicology, 2007, Wright State University

 Sarin is an organophosphorus (OP) ester chemical warfare agent (CWA) that has been used in past terrorist attacks. It remains a threat today because of… (more)

Subjects/Keywords: Health Sciences, Toxicology; sarin; organophosphate; neuroinflammation; neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Davidson, M. E. (2007). Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin Exposure. (Masters Thesis). Wright State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=wright1189715827

Chicago Manual of Style (16th Edition):

Davidson, Molly Elizabeth. “Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin Exposure.” 2007. Masters Thesis, Wright State University. Accessed August 18, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1189715827.

MLA Handbook (7th Edition):

Davidson, Molly Elizabeth. “Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin Exposure.” 2007. Web. 18 Aug 2019.

Vancouver:

Davidson ME. Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin Exposure. [Internet] [Masters thesis]. Wright State University; 2007. [cited 2019 Aug 18]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1189715827.

Council of Science Editors:

Davidson ME. Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin Exposure. [Masters Thesis]. Wright State University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1189715827


Kent State University

14. Renszel, Krystal Marie. USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE.

Degree: MS, College of Arts and Sciences / School of Biomedical Sciences, 2009, Kent State University

 Certain retroviruses are capable of causing progressive spongiform neurodegeneration which results in paralysis, wasting and death; however, the disease mechanism remains unknown. In this study,… (more)

Subjects/Keywords: Biomedical Research; retrovirus; neurodegeneration; protein glycosylation

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Renszel, K. M. (2009). USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE. (Masters Thesis). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent1254659655

Chicago Manual of Style (16th Edition):

Renszel, Krystal Marie. “USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE.” 2009. Masters Thesis, Kent State University. Accessed August 18, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1254659655.

MLA Handbook (7th Edition):

Renszel, Krystal Marie. “USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE.” 2009. Web. 18 Aug 2019.

Vancouver:

Renszel KM. USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE. [Internet] [Masters thesis]. Kent State University; 2009. [cited 2019 Aug 18]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1254659655.

Council of Science Editors:

Renszel KM. USING MUTAGENESIS AND STEM CELLS TO UNDERSTAND RETROVIRAL NEUROVIRULENCE. [Masters Thesis]. Kent State University; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1254659655


Penn State University

15. Robinson, William Foster. Histologic and Electroretinographic Evidence of Diabetes-induced Retinal Neurodegeneration.

Degree: PhD, Anatomy, 2010, Penn State University

 Diabetic retinopathy is a vision-threatening condition, currently affecting more than 5 million Americans. It is the leading cause of new cases of blindness in working-aged… (more)

Subjects/Keywords: diabetes; retinopathy; neurodegeneration; photoreceptor; electroretinography; ERG; immunohistochemistry

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Robinson, W. F. (2010). Histologic and Electroretinographic Evidence of Diabetes-induced Retinal Neurodegeneration. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/11412

Chicago Manual of Style (16th Edition):

Robinson, William Foster. “Histologic and Electroretinographic Evidence of Diabetes-induced Retinal Neurodegeneration.” 2010. Doctoral Dissertation, Penn State University. Accessed August 18, 2019. https://etda.libraries.psu.edu/catalog/11412.

MLA Handbook (7th Edition):

Robinson, William Foster. “Histologic and Electroretinographic Evidence of Diabetes-induced Retinal Neurodegeneration.” 2010. Web. 18 Aug 2019.

Vancouver:

Robinson WF. Histologic and Electroretinographic Evidence of Diabetes-induced Retinal Neurodegeneration. [Internet] [Doctoral dissertation]. Penn State University; 2010. [cited 2019 Aug 18]. Available from: https://etda.libraries.psu.edu/catalog/11412.

Council of Science Editors:

Robinson WF. Histologic and Electroretinographic Evidence of Diabetes-induced Retinal Neurodegeneration. [Doctoral Dissertation]. Penn State University; 2010. Available from: https://etda.libraries.psu.edu/catalog/11412


Penn State University

16. Hall II, Eric Christopher. The contribution of an iron genetic modifier, HFE, to Alzheimer's disease.

Degree: PhD, Neuroscience, 2009, Penn State University

 Alzheimer’s disease (AD) is a neurodegenerative disorder of the human central nervous system characterized by loss of memory that leads to dementia. The pathological characteristics… (more)

Subjects/Keywords: amyloid; neurodegeneration; HFE; iron; tau; pin1

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Hall II, E. C. (2009). The contribution of an iron genetic modifier, HFE, to Alzheimer's disease. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/10189

Chicago Manual of Style (16th Edition):

Hall II, Eric Christopher. “The contribution of an iron genetic modifier, HFE, to Alzheimer's disease.” 2009. Doctoral Dissertation, Penn State University. Accessed August 18, 2019. https://etda.libraries.psu.edu/catalog/10189.

MLA Handbook (7th Edition):

Hall II, Eric Christopher. “The contribution of an iron genetic modifier, HFE, to Alzheimer's disease.” 2009. Web. 18 Aug 2019.

Vancouver:

Hall II EC. The contribution of an iron genetic modifier, HFE, to Alzheimer's disease. [Internet] [Doctoral dissertation]. Penn State University; 2009. [cited 2019 Aug 18]. Available from: https://etda.libraries.psu.edu/catalog/10189.

Council of Science Editors:

Hall II EC. The contribution of an iron genetic modifier, HFE, to Alzheimer's disease. [Doctoral Dissertation]. Penn State University; 2009. Available from: https://etda.libraries.psu.edu/catalog/10189


Kent State University

17. Vignos, Megan C. A HISTOPATHOLOGICAL AND MAGNETIC RESONANCE IMAGING ASSESSMENT OF MYELOCORTICAL MULTIPLE SCLEROSIS: A NEW PATHOLOGICAL VARIANT.

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

 Multiple sclerosis (MS) is an inflammatory-mediated demyelinating, neurodegenerative disease characterized by a diverse clinical course and varying patterns of disease progression. It affects millions of… (more)

Subjects/Keywords: Biomedical Research; Multiple Sclerosis, Histopathology, MRI, Neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Vignos, M. C. (2016). A HISTOPATHOLOGICAL AND MAGNETIC RESONANCE IMAGING ASSESSMENT OF MYELOCORTICAL MULTIPLE SCLEROSIS: A NEW PATHOLOGICAL VARIANT. (Doctoral Dissertation). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent1461528682

Chicago Manual of Style (16th Edition):

Vignos, Megan C. “A HISTOPATHOLOGICAL AND MAGNETIC RESONANCE IMAGING ASSESSMENT OF MYELOCORTICAL MULTIPLE SCLEROSIS: A NEW PATHOLOGICAL VARIANT.” 2016. Doctoral Dissertation, Kent State University. Accessed August 18, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1461528682.

MLA Handbook (7th Edition):

Vignos, Megan C. “A HISTOPATHOLOGICAL AND MAGNETIC RESONANCE IMAGING ASSESSMENT OF MYELOCORTICAL MULTIPLE SCLEROSIS: A NEW PATHOLOGICAL VARIANT.” 2016. Web. 18 Aug 2019.

Vancouver:

Vignos MC. A HISTOPATHOLOGICAL AND MAGNETIC RESONANCE IMAGING ASSESSMENT OF MYELOCORTICAL MULTIPLE SCLEROSIS: A NEW PATHOLOGICAL VARIANT. [Internet] [Doctoral dissertation]. Kent State University; 2016. [cited 2019 Aug 18]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1461528682.

Council of Science Editors:

Vignos MC. A HISTOPATHOLOGICAL AND MAGNETIC RESONANCE IMAGING ASSESSMENT OF MYELOCORTICAL MULTIPLE SCLEROSIS: A NEW PATHOLOGICAL VARIANT. [Doctoral Dissertation]. Kent State University; 2016. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1461528682


University of California – San Diego

18. Gilmore, Stephen. Loss of Nna1 Induces purkinje cell degeneration Through Mitochondrial Dysfunction and Altered Mitochondrial Transport.

Degree: Biology, 2017, University of California – San Diego

 Neurodegenerative Disease is a current and growing health crisis. Recent research into the neurodegenerative disease field has identified mitochondria and microtubules as two systems that… (more)

Subjects/Keywords: Neurosciences; Cellular biology; Microtubules; Mitochondria; Neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Gilmore, S. (2017). Loss of Nna1 Induces purkinje cell degeneration Through Mitochondrial Dysfunction and Altered Mitochondrial Transport. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/0v14c0hv

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):

Gilmore, Stephen. “Loss of Nna1 Induces purkinje cell degeneration Through Mitochondrial Dysfunction and Altered Mitochondrial Transport.” 2017. Thesis, University of California – San Diego. Accessed August 18, 2019. http://www.escholarship.org/uc/item/0v14c0hv.

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

MLA Handbook (7th Edition):

Gilmore, Stephen. “Loss of Nna1 Induces purkinje cell degeneration Through Mitochondrial Dysfunction and Altered Mitochondrial Transport.” 2017. Web. 18 Aug 2019.

Vancouver:

Gilmore S. Loss of Nna1 Induces purkinje cell degeneration Through Mitochondrial Dysfunction and Altered Mitochondrial Transport. [Internet] [Thesis]. University of California – San Diego; 2017. [cited 2019 Aug 18]. Available from: http://www.escholarship.org/uc/item/0v14c0hv.

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

Council of Science Editors:

Gilmore S. Loss of Nna1 Induces purkinje cell degeneration Through Mitochondrial Dysfunction and Altered Mitochondrial Transport. [Thesis]. University of California – San Diego; 2017. Available from: http://www.escholarship.org/uc/item/0v14c0hv

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


University of Southern California

19. Lam, Yeung. Role of neuronal nitric oxide synthase in aging and neurodegeneration.

Degree: PhD, Molecular Pharmacology & Toxicology, 2009, University of Southern California

 Nitric oxide synthase (NOS) is a flavin- and heme- containing enzyme that catalyzes the metabolism of L-arginine to L-citrulline and nitric oxide (.NO) in the… (more)

Subjects/Keywords: neurodegeneration; nitric oxide synthase; nitric oxide; mitochondria

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Lam, Y. (2009). Role of neuronal nitric oxide synthase in aging and neurodegeneration. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/586789/rec/5638

Chicago Manual of Style (16th Edition):

Lam, Yeung. “Role of neuronal nitric oxide synthase in aging and neurodegeneration.” 2009. Doctoral Dissertation, University of Southern California. Accessed August 18, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/586789/rec/5638.

MLA Handbook (7th Edition):

Lam, Yeung. “Role of neuronal nitric oxide synthase in aging and neurodegeneration.” 2009. Web. 18 Aug 2019.

Vancouver:

Lam Y. Role of neuronal nitric oxide synthase in aging and neurodegeneration. [Internet] [Doctoral dissertation]. University of Southern California; 2009. [cited 2019 Aug 18]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/586789/rec/5638.

Council of Science Editors:

Lam Y. Role of neuronal nitric oxide synthase in aging and neurodegeneration. [Doctoral Dissertation]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/586789/rec/5638


University of Illinois – Chicago

20. Braun, David J. Damage to the Locus Coeruleus in Alzheimer's Disease: Potential Causes and Therapeutic Targets.

Degree: 2016, University of Illinois – Chicago

 Therapeutic options for Alzheimer's disease (AD) are limited, and this dearth of treatments necessitates the development of novel therapeutic targets. One such target is the… (more)

Subjects/Keywords: noradrenaline; locus coeruleus; Alzheimer's disease; neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Braun, D. J. (2016). Damage to the Locus Coeruleus in Alzheimer's Disease: Potential Causes and Therapeutic Targets. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/21206

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):

Braun, David J. “Damage to the Locus Coeruleus in Alzheimer's Disease: Potential Causes and Therapeutic Targets.” 2016. Thesis, University of Illinois – Chicago. Accessed August 18, 2019. http://hdl.handle.net/10027/21206.

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

MLA Handbook (7th Edition):

Braun, David J. “Damage to the Locus Coeruleus in Alzheimer's Disease: Potential Causes and Therapeutic Targets.” 2016. Web. 18 Aug 2019.

Vancouver:

Braun DJ. Damage to the Locus Coeruleus in Alzheimer's Disease: Potential Causes and Therapeutic Targets. [Internet] [Thesis]. University of Illinois – Chicago; 2016. [cited 2019 Aug 18]. Available from: http://hdl.handle.net/10027/21206.

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

Council of Science Editors:

Braun DJ. Damage to the Locus Coeruleus in Alzheimer's Disease: Potential Causes and Therapeutic Targets. [Thesis]. University of Illinois – Chicago; 2016. Available from: http://hdl.handle.net/10027/21206

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


University of South Florida

21. Finneran, Dylan John. Proteolysis of CX3CL1 Impacts CX3CR1 Signaling and Therapeutic Benefits in a Tauopathy Model.

Degree: 2018, University of South Florida

 Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder and the most common form of dementia. The hallmark pathologies of AD are extracellular aggregates of amyloid-beta,… (more)

Subjects/Keywords: Alzheimer's disease; Fractalkine; Microglia; Neurodegeneration; Neuroinflammation; Neurosciences

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Finneran, D. J. (2018). Proteolysis of CX3CL1 Impacts CX3CR1 Signaling and Therapeutic Benefits in a Tauopathy Model. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/7504

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):

Finneran, Dylan John. “Proteolysis of CX3CL1 Impacts CX3CR1 Signaling and Therapeutic Benefits in a Tauopathy Model.” 2018. Thesis, University of South Florida. Accessed August 18, 2019. https://scholarcommons.usf.edu/etd/7504.

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

MLA Handbook (7th Edition):

Finneran, Dylan John. “Proteolysis of CX3CL1 Impacts CX3CR1 Signaling and Therapeutic Benefits in a Tauopathy Model.” 2018. Web. 18 Aug 2019.

Vancouver:

Finneran DJ. Proteolysis of CX3CL1 Impacts CX3CR1 Signaling and Therapeutic Benefits in a Tauopathy Model. [Internet] [Thesis]. University of South Florida; 2018. [cited 2019 Aug 18]. Available from: https://scholarcommons.usf.edu/etd/7504.

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

Council of Science Editors:

Finneran DJ. Proteolysis of CX3CL1 Impacts CX3CR1 Signaling and Therapeutic Benefits in a Tauopathy Model. [Thesis]. University of South Florida; 2018. Available from: https://scholarcommons.usf.edu/etd/7504

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


Boston University

22. Labadorf, Adam. Characterizing the Huntington's disease, Parkinson's disease, and pan-neurodegenerative gene expression signature with RNA sequencing.

Degree: PhD, Bioinformatics GRS, 2016, Boston University

 Huntington's disease (HD) and Parkinson's disease (PD) are devastating neurodegenerative disorders that are characterized pathologically by degeneration of neurons in the brain and clinically by… (more)

Subjects/Keywords: Bioinformatics; Genomics; Neurodegeneration; Huntington's disease; Parkinson's disease

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Labadorf, A. (2016). Characterizing the Huntington's disease, Parkinson's disease, and pan-neurodegenerative gene expression signature with RNA sequencing. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/17865

Chicago Manual of Style (16th Edition):

Labadorf, Adam. “Characterizing the Huntington's disease, Parkinson's disease, and pan-neurodegenerative gene expression signature with RNA sequencing.” 2016. Doctoral Dissertation, Boston University. Accessed August 18, 2019. http://hdl.handle.net/2144/17865.

MLA Handbook (7th Edition):

Labadorf, Adam. “Characterizing the Huntington's disease, Parkinson's disease, and pan-neurodegenerative gene expression signature with RNA sequencing.” 2016. Web. 18 Aug 2019.

Vancouver:

Labadorf A. Characterizing the Huntington's disease, Parkinson's disease, and pan-neurodegenerative gene expression signature with RNA sequencing. [Internet] [Doctoral dissertation]. Boston University; 2016. [cited 2019 Aug 18]. Available from: http://hdl.handle.net/2144/17865.

Council of Science Editors:

Labadorf A. Characterizing the Huntington's disease, Parkinson's disease, and pan-neurodegenerative gene expression signature with RNA sequencing. [Doctoral Dissertation]. Boston University; 2016. Available from: http://hdl.handle.net/2144/17865


University of Miami

23. Carlson, Nicole E. Ras Opposite, the Drosophila Homologue of Munc18-1, is Important for Motor Axon Maintenance.

Degree: MS, Neuroscience (Medicine), 2011, University of Miami

 Amyotrophic Lateral Sclerosis (ALS) is a fatal disease characterized by the progressive degeneration of motor neurons. Although there has been some progress in the identification… (more)

Subjects/Keywords: Rop; Munc18; ALS; neurodegeneration; Drosophila; motor neurons

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Carlson, N. E. (2011). Ras Opposite, the Drosophila Homologue of Munc18-1, is Important for Motor Axon Maintenance. (Thesis). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_theses/242

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):

Carlson, Nicole E. “Ras Opposite, the Drosophila Homologue of Munc18-1, is Important for Motor Axon Maintenance.” 2011. Thesis, University of Miami. Accessed August 18, 2019. https://scholarlyrepository.miami.edu/oa_theses/242.

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

MLA Handbook (7th Edition):

Carlson, Nicole E. “Ras Opposite, the Drosophila Homologue of Munc18-1, is Important for Motor Axon Maintenance.” 2011. Web. 18 Aug 2019.

Vancouver:

Carlson NE. Ras Opposite, the Drosophila Homologue of Munc18-1, is Important for Motor Axon Maintenance. [Internet] [Thesis]. University of Miami; 2011. [cited 2019 Aug 18]. Available from: https://scholarlyrepository.miami.edu/oa_theses/242.

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

Council of Science Editors:

Carlson NE. Ras Opposite, the Drosophila Homologue of Munc18-1, is Important for Motor Axon Maintenance. [Thesis]. University of Miami; 2011. Available from: https://scholarlyrepository.miami.edu/oa_theses/242

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


Florida International University

24. Valdes, James J. Estrogen and Lithium: Facilitating Factors Involved in Brain Cell Signaling Pathways.

Degree: Biology, 2009, Florida International University

  Learning and memory in adult females decline during menopause and estrogen replacement therapy is commonly prescribed during menopause. Post-menopausal women tend to suffer from… (more)

Subjects/Keywords: estrogen; lithium; brain; learning; memory; neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Valdes, J. J. (2009). Estrogen and Lithium: Facilitating Factors Involved in Brain Cell Signaling Pathways. (Thesis). Florida International University. Retrieved from http://digitalcommons.fiu.edu/etd/105 ; 10.25148/etd.FI09120801 ; FI09120801

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):

Valdes, James J. “Estrogen and Lithium: Facilitating Factors Involved in Brain Cell Signaling Pathways.” 2009. Thesis, Florida International University. Accessed August 18, 2019. http://digitalcommons.fiu.edu/etd/105 ; 10.25148/etd.FI09120801 ; FI09120801.

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

MLA Handbook (7th Edition):

Valdes, James J. “Estrogen and Lithium: Facilitating Factors Involved in Brain Cell Signaling Pathways.” 2009. Web. 18 Aug 2019.

Vancouver:

Valdes JJ. Estrogen and Lithium: Facilitating Factors Involved in Brain Cell Signaling Pathways. [Internet] [Thesis]. Florida International University; 2009. [cited 2019 Aug 18]. Available from: http://digitalcommons.fiu.edu/etd/105 ; 10.25148/etd.FI09120801 ; FI09120801.

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

Council of Science Editors:

Valdes JJ. Estrogen and Lithium: Facilitating Factors Involved in Brain Cell Signaling Pathways. [Thesis]. Florida International University; 2009. Available from: http://digitalcommons.fiu.edu/etd/105 ; 10.25148/etd.FI09120801 ; FI09120801

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


Vanderbilt University

25. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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://etd.library.vanderbilt.edu/available/etd-03232018-135223/ ;

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 August 18, 2019. http://etd.library.vanderbilt.edu/available/etd-03232018-135223/ ;.

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. 18 Aug 2019.

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 2019 Aug 18]. Available from: http://etd.library.vanderbilt.edu/available/etd-03232018-135223/ ;.

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://etd.library.vanderbilt.edu/available/etd-03232018-135223/ ;


Boston University

26. Wang, Hao. The role of matrin 3 in the pathogenesis of amyotrophic lateral sclerosis.

Degree: MS, Medical Sciences and Public Health GMS, 2015, Boston University

 The cause of amyotrophic lateral sclerosis (ALS), a cruel neurodegenerative disease, remains unclear. Trans-activating response region (TAR) DNA-binding protein of 43 kDa (TDP-43) has been… (more)

Subjects/Keywords: Pharmacology; ALS; MATR3; Matrin 3; TDP43; Neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Wang, H. (2015). The role of matrin 3 in the pathogenesis of amyotrophic lateral sclerosis. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16177

Chicago Manual of Style (16th Edition):

Wang, Hao. “The role of matrin 3 in the pathogenesis of amyotrophic lateral sclerosis.” 2015. Masters Thesis, Boston University. Accessed August 18, 2019. http://hdl.handle.net/2144/16177.

MLA Handbook (7th Edition):

Wang, Hao. “The role of matrin 3 in the pathogenesis of amyotrophic lateral sclerosis.” 2015. Web. 18 Aug 2019.

Vancouver:

Wang H. The role of matrin 3 in the pathogenesis of amyotrophic lateral sclerosis. [Internet] [Masters thesis]. Boston University; 2015. [cited 2019 Aug 18]. Available from: http://hdl.handle.net/2144/16177.

Council of Science Editors:

Wang H. The role of matrin 3 in the pathogenesis of amyotrophic lateral sclerosis. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16177


University of Minnesota

27. Holmay, Mary. Pharmacology and Clinical Effects of N-acetylcysteine in Neurodegenerative Disorders.

Degree: PhD, Experimental & Clinical Pharmacology, 2015, University of Minnesota

 Free radicals and other reactive oxygen species (ROS) constitute a normal part of the intracellular environment. Endogenous enzymes such as catalase, superoxide dismutase and the… (more)

Subjects/Keywords: antioxidant; glutathione; neurodegeneration; Oxidative stress; pharmacology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Holmay, M. (2015). Pharmacology and Clinical Effects of N-acetylcysteine in Neurodegenerative Disorders. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/191347

Chicago Manual of Style (16th Edition):

Holmay, Mary. “Pharmacology and Clinical Effects of N-acetylcysteine in Neurodegenerative Disorders.” 2015. Doctoral Dissertation, University of Minnesota. Accessed August 18, 2019. http://hdl.handle.net/11299/191347.

MLA Handbook (7th Edition):

Holmay, Mary. “Pharmacology and Clinical Effects of N-acetylcysteine in Neurodegenerative Disorders.” 2015. Web. 18 Aug 2019.

Vancouver:

Holmay M. Pharmacology and Clinical Effects of N-acetylcysteine in Neurodegenerative Disorders. [Internet] [Doctoral dissertation]. University of Minnesota; 2015. [cited 2019 Aug 18]. Available from: http://hdl.handle.net/11299/191347.

Council of Science Editors:

Holmay M. Pharmacology and Clinical Effects of N-acetylcysteine in Neurodegenerative Disorders. [Doctoral Dissertation]. University of Minnesota; 2015. Available from: http://hdl.handle.net/11299/191347


Penn State University

28. Peters, Douglas. NOVEL MODEL FOR LOADING BRAIN IRON IN MICE: IMPLICATIONS FOR STUDYING AGING AND AMYLOID PATHOLOGY.

Degree: 2017, Penn State University

 Brain iron accumulation occurs normally in the aging brain to facilitate myelination of white matter (WM); neurotransmitter synthesis; and ATP production. However, mishandling of iron… (more)

Subjects/Keywords: Alzheimer's disease; Iron; Aging; MRI; Histology; Neurodegeneration

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Peters, D. (2017). NOVEL MODEL FOR LOADING BRAIN IRON IN MICE: IMPLICATIONS FOR STUDYING AGING AND AMYLOID PATHOLOGY. (Thesis). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/14665dzp146

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):

Peters, Douglas. “NOVEL MODEL FOR LOADING BRAIN IRON IN MICE: IMPLICATIONS FOR STUDYING AGING AND AMYLOID PATHOLOGY.” 2017. Thesis, Penn State University. Accessed August 18, 2019. https://etda.libraries.psu.edu/catalog/14665dzp146.

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

MLA Handbook (7th Edition):

Peters, Douglas. “NOVEL MODEL FOR LOADING BRAIN IRON IN MICE: IMPLICATIONS FOR STUDYING AGING AND AMYLOID PATHOLOGY.” 2017. Web. 18 Aug 2019.

Vancouver:

Peters D. NOVEL MODEL FOR LOADING BRAIN IRON IN MICE: IMPLICATIONS FOR STUDYING AGING AND AMYLOID PATHOLOGY. [Internet] [Thesis]. Penn State University; 2017. [cited 2019 Aug 18]. Available from: https://etda.libraries.psu.edu/catalog/14665dzp146.

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

Council of Science Editors:

Peters D. NOVEL MODEL FOR LOADING BRAIN IRON IN MICE: IMPLICATIONS FOR STUDYING AGING AND AMYLOID PATHOLOGY. [Thesis]. Penn State University; 2017. Available from: https://etda.libraries.psu.edu/catalog/14665dzp146

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


University of California – San Francisco

29. Robertson, Dana Katherine. Effect of ethanol on protein quality control: implications for aging and degenerative disease.

Degree: Neuroscience, 2011, University of California – San Francisco

 The main protein quality control systems, the ubiquitin-proteasome system and macroautophagy, have been implicated in a diverse range of neurodegenerative disease as well as alcoholic… (more)

Subjects/Keywords: Neurosciences; Aging; Autophagy; Ethanol; Neurodegeneration; PQC; Proteasome

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Robertson, D. K. (2011). Effect of ethanol on protein quality control: implications for aging and degenerative disease. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/7xw6w07j

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):

Robertson, Dana Katherine. “Effect of ethanol on protein quality control: implications for aging and degenerative disease.” 2011. Thesis, University of California – San Francisco. Accessed August 18, 2019. http://www.escholarship.org/uc/item/7xw6w07j.

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

MLA Handbook (7th Edition):

Robertson, Dana Katherine. “Effect of ethanol on protein quality control: implications for aging and degenerative disease.” 2011. Web. 18 Aug 2019.

Vancouver:

Robertson DK. Effect of ethanol on protein quality control: implications for aging and degenerative disease. [Internet] [Thesis]. University of California – San Francisco; 2011. [cited 2019 Aug 18]. Available from: http://www.escholarship.org/uc/item/7xw6w07j.

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

Council of Science Editors:

Robertson DK. Effect of ethanol on protein quality control: implications for aging and degenerative disease. [Thesis]. University of California – San Francisco; 2011. Available from: http://www.escholarship.org/uc/item/7xw6w07j

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


University of California – San Francisco

30. Hauswirth, Anna Genevieve Bhat. Presynaptic Homeostatic Plasticity in Health and Disease.

Degree: Neuroscience, 2017, University of California – San Francisco

 Homeostatic plasticity mechanisms stabilize neural function in organisms ranging from insect to human. One form, presynaptic homeostatic potentiation (PHP), rapidly stabilizes postsynaptic excitation following postsynaptic… (more)

Subjects/Keywords: Neurosciences; homeostatic plasticity; neurodegeneration; PI3-kinases

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Hauswirth, A. G. B. (2017). Presynaptic Homeostatic Plasticity in Health and Disease. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/02c1c2v2

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):

Hauswirth, Anna Genevieve Bhat. “Presynaptic Homeostatic Plasticity in Health and Disease.” 2017. Thesis, University of California – San Francisco. Accessed August 18, 2019. http://www.escholarship.org/uc/item/02c1c2v2.

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

MLA Handbook (7th Edition):

Hauswirth, Anna Genevieve Bhat. “Presynaptic Homeostatic Plasticity in Health and Disease.” 2017. Web. 18 Aug 2019.

Vancouver:

Hauswirth AGB. Presynaptic Homeostatic Plasticity in Health and Disease. [Internet] [Thesis]. University of California – San Francisco; 2017. [cited 2019 Aug 18]. Available from: http://www.escholarship.org/uc/item/02c1c2v2.

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

Council of Science Editors:

Hauswirth AGB. Presynaptic Homeostatic Plasticity in Health and Disease. [Thesis]. University of California – San Francisco; 2017. Available from: http://www.escholarship.org/uc/item/02c1c2v2

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

[1] [2] [3] [4] [5] [6] [7] [8] [9]

.