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Calpain Cleavage of GAD65 is pathological and impairs gaba neurotransmission
Title
Calpain Cleavage of GAD65 is pathological and impairs gaba neurotransmission.
Creator
Buddhala, Chandana, Suarez, Marjorie, Alexandrescu, Anamaria, Pissaris, Adam, Modi, Jigar P., Wei, Jianning, Prentice, Howard, Wu, Jang-Yen, Graduate College
Date Issued
2011-04-08
PURL
http://purl.flvc.org/fcla/dt/3164511
Subject Headings
Nervous System Diseases, GABA --physiology, Gamma-aminoboterzuur
Format
Document (PDF)
KLEINE-LEVIN SYNDROME: INVESTIGATING THE IMMUNO-REACTIVITY OF PATIENT SERA TOWARDS VARIOUS BRAIN AREAS
Title
KLEINE-LEVIN SYNDROME: INVESTIGATING THE IMMUNO-REACTIVITY OF PATIENT SERA TOWARDS VARIOUS BRAIN AREAS.
Creator
Hamper, Michael C., Wei, Jianning, Hartmann, James, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Abstract/Description
Kleine-Levin Syndrome (KLS) is an extremely rare neurological disorder characterized by episodes of uncontrollable hypersomnia and various cognitive and behavioral abnormalities. There is neither a definitive etiology nor definite treatment modalities. Immunological studies for this condition are extremely limited, and this present study aims to investigate a potential autoimmune mechanism that underlies KLS. To achieve this, western blot and dot-blot assays analyzed the immunoreactivity of...
Show moreKleine-Levin Syndrome (KLS) is an extremely rare neurological disorder characterized by episodes of uncontrollable hypersomnia and various cognitive and behavioral abnormalities. There is neither a definitive etiology nor definite treatment modalities. Immunological studies for this condition are extremely limited, and this present study aims to investigate a potential autoimmune mechanism that underlies KLS. To achieve this, western blot and dot-blot assays analyzed the immunoreactivity of patients and control sera towards various brain tissue areas. Western blot did not show immunoreactivity with IgG-depleted brain tissue lysate. However, dot-blot assays revealed a significantly greater level of immunoreactivity with KLS patient sera towards the dorsolateral prefrontal cortex, hypothalamus, and parieto-temporal areas compared to KLS-negative sera. These areas have previously been shown to be hypo-perfused in KLS patients. Future studies are necessary to identify the specific antibodies that may be autoreactive in KLS patients.
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Date Issued
2023
PURL
http://purl.flvc.org/fau/fd/FA00014359
Subject Headings
Kleine-Levin Syndrome, Autoantibodies, Hypersomnia, Nervous System Diseases
Format
Document (PDF)
GABAERGIC NEUROTRANSMISSION AND POTENTIAL RESCUE METHODS FROM CHEMOTHERAPY-INDUCED PERIPHERAL NEUROPATHIES IN C. ELEGANS
Title
GABAERGIC NEUROTRANSMISSION AND POTENTIAL RESCUE METHODS FROM CHEMOTHERAPY-INDUCED PERIPHERAL NEUROPATHIES IN C. ELEGANS.
Creator
Gonzalez-Lerma, Paola X., Dawson-Scully, Kenneth, Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
Abstract/Description
Cancer is a leading cause of death in the U.S and across the world, with estimates indicating 17 million new cancer cases in 2018, 9.5 million of which resulted in death. Statistics show that in the past 20 years cancer death rates have decreased 27% due to emerging therapies. The use of chemotherapies to kill fast-growing cells in the body has become one of the most common cancer treatments in the world today. Chemotherapy-Induced Peripheral Neuropathies (CIPNs) are the most common side...
Show moreCancer is a leading cause of death in the U.S and across the world, with estimates indicating 17 million new cancer cases in 2018, 9.5 million of which resulted in death. Statistics show that in the past 20 years cancer death rates have decreased 27% due to emerging therapies. The use of chemotherapies to kill fast-growing cells in the body has become one of the most common cancer treatments in the world today. Chemotherapy-Induced Peripheral Neuropathies (CIPNs) are the most common side effects caused by chemotherapeutic agents. CIPNs have a prevalence of up to 85% in cancer patients undergoing chemotherapy. CIPNs triggered by chemotherapeutic drug use severely damage nerves branching from either the brain or spinal cord, initiating the development of acute and/or chronic symptoms. Platinum-based and taxane-based chemotherapeutics are among the most potent and versatile drugs available for combating cancer. The two of these drugs, carboplatin and docetaxel, are known to cause peripheral neuropathies and central neurotoxicity and were the focus of this project.
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Date Issued
2024
PURL
http://purl.flvc.org/fau/fd/FA00014450
Subject Headings
Peripheral Nervous System Diseases, Chemotherapy, Caenorhabditis elegans, Cancer
Format
Document (PDF)
study on neural conduction as in myelinated structure under pathological conditions
Title
A study on neural conduction as in myelinated structure under pathological conditions.
Creator
Morales, George J., College of Engineering and Computer Science, Department of Computer and Electrical Engineering and Computer Science
Abstract/Description
A method for modeling and simulating neural action potential (AP) propagation along the length of an axon containing a number of Ranvier nodes is proposed in this dissertation. A system identification approach is adopted to represent node of Ranvier (NR) response to current pulse stimulus in the form of transfer function representations for NR excitability. Segments of myelinated internodal (IN) and NR regions are cascaded, representing the remaining downstream axon after a site-of-stimulus...
Show moreA method for modeling and simulating neural action potential (AP) propagation along the length of an axon containing a number of Ranvier nodes is proposed in this dissertation. A system identification approach is adopted to represent node of Ranvier (NR) response to current pulse stimulus in the form of transfer function representations for NR excitability. Segments of myelinated internodal (IN) and NR regions are cascaded, representing the remaining downstream axon after a site-of-stimulus introduction of an external current pulse. This cascading network is used to simulate "cable" properties and signal propagation along the length of the axon. This work proposes possible solutions to attenuation losses inherited in the classical myelinated cable models and accounts for neuronal AP velocity as well as introducing signal attenuation and transient delays associated with internodal demyelination. This model could aide as a predictive tool for the diagnosis and analysis of axonal signal integrity associated with demyelination pathology. Possible applications could include functional stimulation control methodologies for axon bundles that may exhibit signal fidelity issues associated with demyelination. It is further proposed that this model may serve as an instructive tool for further development and incorporation of other axon dynamic behaviors such as: relative refractory periods of AP generation, NR AP recovery mechanisms and responses to varied current stimulus input.
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Date Issued
2011
PURL
http://purl.flvc.org/FAU/3171723
Subject Headings
Nervous system, Diseases, Research, Demyelination, Nodes of Ranvier, Neuromuscular diseases, Research
Format
Document (PDF)
use of novel HDACi's for treatment of memory impairment in a mouse model of Alzheimer's disease
Title
The use of novel HDACi's for treatment of memory impairment in a mouse model of Alzheimer's disease.
Creator
Moyes, Jonathan., Harriet L. Wilkes Honors College
Abstract/Description
Alzheimer's disease (AD) is an increasingly common neurological disorder that mainly affects memory formation and retention. It is characterized by unique intercellular neurofibrillary tangles and extracellular beta-amyloid plaques. Histone deacetylase inhibitors (HDACi's) are competitive antagonists against histone deacetylases, causing histone acetyltransferases to acetylate the genome unregulated. This thesis investigates the use of new histone deacetylase inhibitors on recovering memory...
Show moreAlzheimer's disease (AD) is an increasingly common neurological disorder that mainly affects memory formation and retention. It is characterized by unique intercellular neurofibrillary tangles and extracellular beta-amyloid plaques. Histone deacetylase inhibitors (HDACi's) are competitive antagonists against histone deacetylases, causing histone acetyltransferases to acetylate the genome unregulated. This thesis investigates the use of new histone deacetylase inhibitors on recovering memory in a mouse model of Alzheimer's disease. By use of a fear conditioning paradigm, we have shown that these HDACI's increase memory in AD mice, but show either no effect or a positive effect in wild-type mice. Future experiments will investigate the efficacy of compound 966 and the spine density of hippocampal brain slices after fear conditioning trials.
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Date Issued
2012
PURL
http://purl.flvc.org/FAU/3359315
Subject Headings
Alzheimer's disease, Chemotherapy, Pharmacogenetics, Histone deacetylase, Inhibitors, Nervous system, Degeneration, Molecular aspects
Format
Document (PDF)
Neuroprotection from induced glutamate excitotoxicity by Conus brunneus conopeptides in a stroke-related model
Title
Neuroprotection from induced glutamate excitotoxicity by Conus brunneus conopeptides in a stroke-related model.
Creator
Crouch, Rebecca A., Charles E. Schmidt College of Science, Department of Chemistry and Biochemistry
Abstract/Description
Cone snails are carnivorous marine mollusks, utilizing their neuropeptide-rich venom for prey capture. The venom of Conus brunneus, a wide-spread Eastern Pacific vermivore, has not been extensively studied. In the current work, peptides from the dissected venom were characterized and tested using preliminary bioassays. Six peptides (A-F) were isolated and tested. Three peptide identities were determined by comparison with previously reported data: bru9a (A), bru3a (F), and an a-conotoxin (E)....
Show moreCone snails are carnivorous marine mollusks, utilizing their neuropeptide-rich venom for prey capture. The venom of Conus brunneus, a wide-spread Eastern Pacific vermivore, has not been extensively studied. In the current work, peptides from the dissected venom were characterized and tested using preliminary bioassays. Six peptides (A-F) were isolated and tested. Three peptide identities were determined by comparison with previously reported data: bru9a (A), bru3a (F), and an a-conotoxin (E). Preliminary screening in a stroke-related model of induced glutamate excitotoxicity in primary neuronal cells and PC12 cell cultures indicated potential neuroprotective activity of peptide fractions A, D, and F. Further testing is necessary to determine and verify structure, activity, target, and mechanism of action of the promising peptides from C. brunneus, which may prove effective neuropharmacological agents to treat stroke.
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Date Issued
2013
PURL
http://purl.flvc.org/fcla/dt/3362331
Subject Headings
Gastropoda, Venom, Therapeutic use, Peptides, Structure, Neuroprotective agents, Central nervous system, Diseases, Treatment
Format
Document (PDF)
Polyglutamine aggregates stimulate ER stress and trigger apoptosis by activating BH-3 only protein Bim
Title
Polyglutamine aggregates stimulate ER stress and trigger apoptosis by activating BH-3 only protein Bim.
Creator
Bhagavatula, Nithya, Wei, Jianning, Florida Atlantic University
Abstract/Description
Huntington's disease (HD) is an inherited neurological disorder characterized by a selective loss of neurons in the striatum and cortex leading to involuntary movement, dementia and eventually cell death. HD is caused by an expanded polyglutamine (PolyQ) repeat in Huntingtin (Htt) protein. It is well known that misfolded mutant Htt could form intracellular aggregates, trigger ER stress and ultimately lead to apoptosis. However, the molecular link between ER stress and apoptosis in...
Show moreHuntington's disease (HD) is an inherited neurological disorder characterized by a selective loss of neurons in the striatum and cortex leading to involuntary movement, dementia and eventually cell death. HD is caused by an expanded polyglutamine (PolyQ) repeat in Huntingtin (Htt) protein. It is well known that misfolded mutant Htt could form intracellular aggregates, trigger ER stress and ultimately lead to apoptosis. However, the molecular link between ER stress and apoptosis in mitochondria is poorly understood. In the present study, we identified Bim (Bcl-2 interacting mediator of cell death) as the essential protein. We first established a cellular model of HD by over expressing the Nterminus of wild type and mutant Htt into HEK293 cell lines. We showed that the accumulation and aggregation of misfolded mutant Htt protein triggers ER stress and apoptosis. The Bim protein expression level was greatly increased in mutant Htt transfected cells and this increase was partially due to up-regulation of Bim mRNA as analyzed using quantitative RT-PCR. We further showed that Bim phosphorylation also played an important role in regulating Bim expression. Moreover, up-regulation of Bim facilitates the translocation of Bax to mitochondrial membrane, which lead to cytochrome c release and apoptosis. We also silenced Bim using siRNA to further investigate the essential role of Bim in mutant Htt induced ER stress and apoptosis. Identifying the Bim pathway that is altered in response to the mutant Htt protein is important for understanding the cellular processes impacted by the disease.
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Date Issued
2008
PURL
http://purl.flvc.org/fau/fd/FA00000726
Subject Headings
Nervous system--Degeneration--Molecular aspects, Apoptosis, Cellular signal transduction, Huntington's disease--Genetic aspects, Huntington's disease--Pathophysiology
Format
Document (PDF)
The synergistic effects of concurrent stress on the inflammatory response in healthy individuals
Title
The synergistic effects of concurrent stress on the inflammatory response in healthy individuals.
Creator
McAlpine, David, Huang, Chun-Jung
Date Issued
2012-04-06
PURL
http://purl.flvc.org/fcla/dt/3349030
Subject Headings
Pentraxin 3, Inflammation, PTX3 protein, Vascular Diseases, Blood Vessels, C-Reactive Protein, Inflammation --blod, Parasympathetic Nervous System, Stress --psychological
Format
Document (PDF)
Over-Expression of BDNF Does Not Rescue Sensory Deprivation-Induced Death of Adult-Born Olfactory Granule Cells
Title
Over-Expression of BDNF Does Not Rescue Sensory Deprivation-Induced Death of Adult-Born Olfactory Granule Cells.
Creator
Berger, Rachel A., Guthrie, Kathleen M., Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description
It is of interest to understand how new neurons incorporate themselves into the existing circuitry of certain neuronal populations. One such population of neurons is that which are born in the subventricular zone (SVZ) and migrate to the olfactory bulb where they differentiate into granule cells. Another area of interest is the role of brain-derived neurotrophic factor (BDNF) on the survival and overall health of these neurons. This study aimed to test whether or not BDNF is a survival factor...
Show moreIt is of interest to understand how new neurons incorporate themselves into the existing circuitry of certain neuronal populations. One such population of neurons is that which are born in the subventricular zone (SVZ) and migrate to the olfactory bulb where they differentiate into granule cells. Another area of interest is the role of brain-derived neurotrophic factor (BDNF) on the survival and overall health of these neurons. This study aimed to test whether or not BDNF is a survival factor for adult-born granule cells. Here were utilized a transgenic mouse model over-expressing BDNF under the α- calcium/calmodulin-dependent protein kinase II (CAMKIIα) promoter, and tested its effect on olfactory granule cells under sensory deprived conditions. Results from this experiment indicated that there was no significant difference in cell death or cell survival when comparing transgenic and wild type animals. We concluded that BDNF is not a survival factor for adult-born granule cells.
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Date Issued
2016
PURL
http://purl.flvc.org/fau/fd/FA00004722, http://purl.flvc.org/fau/fd/FA00004722
Subject Headings
Cellular control mechanisms, Mice as laboratory animals, Nervous system -- Diseases -- Gene therapy, Neural circuitry, Neuroplasticity, Neurotransmitter receptors, Sensory deprivation, Sensory neurons -- Testing
Format
Document (PDF)