Nervous System Diseases Commons^™

Validation Of A Serotonin Depletion Checklist In Parkinson’S Disease, Kelly Diane Darby Holder

Loma Linda University Electronic Theses, Dissertations & Projects

The distinctive pathological marker of Parkinson’s Disease (PD) is the progressive death of neurons that produce dopamine; however, there are also major alterations in the production of quantities of other neurotransmitters, such as norepinephrine and serotonin that contribute to the signs, symptoms, neuropsychological manifestations of the diseases. PD patients can be divided into classes based on the manifestation of motor symptoms, type A, classified as tremor dominant, and type B PD, classified as akinetic. Type B PD patients, often manifest symptoms in which serotonin deficiency plays an important role, such as frontal cognitive impairments, which often includes a history of …

Gene Therapy And Targeted Toxins For Glioma, James Curtin, Gwendalyn King, Marianela Candolfi, Kurt Kroeger, Pedro Lowenstein, Maria Castro

Articles

The most common primary brain tumor in adults is glioblastoma. These tumors are highly invasive and aggressive with a mean survival time of nine to twelve months from diagnosis to death. Current treatment modalities are unable to significantly prolong survival in patients diagnosed with glioblastoma. As such, glioma is an attractive target for developing novel therapeutic approaches utilizing gene therapy. This review will examine the available preclinical models for glioma including xenographs, syngeneic and genetic models. Several promising therapeutic targets are currently being pursued in pre-clinical investigations. These targets will be reviewed by mechanism of action, i.e., conditional cytotoxic, targeted …

Combining Cytotoxic And Immune-Mediated Gene Therapy To Treat Brain Tumors, James Curtin, Gwendalyn King, Marianela Candolfi, Remy Greeno, Kurt Kroeger, Pedro Lowenstein, Maria Castro

Articles

Glioblastoma (GBM) is a type of intracranial brain tumor, for which there is no cure. In spite of advances in surgery, chemotherapy and radiotherapy, patients die within a year of diagnosis. Therefore, there is a critical need to develop novel therapeutic approaches for this disease. Gene therapy, which is the use of genes or other nucleic acids as drugs, is a powerful new treatment strategy which can be developed to treat GBM. Several treatment modalities are amenable for gene therapy implementation, e.g. conditional cytotoxic approaches, targeted delivery of toxins into the tumor mass, immune stimulatory strategies, and these will all …

Regulation Of Proto-Oncogenes Expression In Developmental Epilepsy, Mahnoush Shafiei

Seton Hall University Dissertations and Theses (ETDs)

Seizures cause selective neuronal cell loss in vulnerable regions such as the hippocampus, cortex, thalamus or substantia nigra (SN) in human or experimental animals. While the HF can propagate seizures, the SN pars reticulata (SNR) regulates the spread ol seizures in an age-dependent fashion, and the pars compacta (SNC) affects extrapyramidal motor control. In mature animals, both structures are wlnerable to seizure-induced damage. In prepubescent rats, seizure susceptibility is reduced and CA 1 region rs primarily affected. The proto-oncogenes, Bcl-2 and Bax, encode specific proteins that inhibit and promote programmed cell death, respectively. In order to determine whether proto-oncogenes are …

Neuronal And Metabolic Increases In Pedunculopontine Nucleus Of Parkinson's Rats, Jonathan Dennis Carlson

Loma Linda University Electronic Theses, Dissertations & Projects

The theoretical mechanisms underlying the symptoms of Parkinson’s disease are based on dysfunctional output from the basal ganglia projected to the cortex via the thalamus. However, the subthalamic nucleus (STN) and substantia nigra pars reticularis (SNr) as part of the basal ganglia, also project to the brainstem, in particular to the pedunculopontine nucleus (PPN). Both the STN and SNr have altered neuronal activity in the 6-hydroxydopamine (6-OHDA) Parkinson’s model rat. Thus, it is hypothesized that the PPN is altered in this model of Parkinson’s disease.

This hypothesis was examined by comparing the rates of glucose metabolism and spontaneous neuronal activity …

Increased Glutathione Metabolic Defense Capabilities In Cultured Alzheimer's Diseased Lymphoblast Cell Lines, Collin M. Shaw

Dissertations and Theses

The hypothesis to be tested states that the pathology of Alzheimer's disease (AD) involves elevated levels of oxidative stress, resulting in elevated levels of cellular oxidative defense mechanisms. If the premise is true, than AD pathologically afflicted cells should have a higher demand for glutathione (GSH) as an innate oxidative defense mechanism hence; greater GSH concentrations, increased GSH resynthesis capabilities, and increased levels of cystathionine gamma-lyase (CNase). Alzheimer diseased and age matched control lymphoblast cells, obtained from OHSU's Oregon Brain Aging Study, were cultured, and GSH biochemistry was subsequently evaluated. GSH was depleted by exposing cells to the GSH depleting …

Analysis Of Serotonin And Postural Instability In Parkinson’S Disease, Sandra Kuniyoshi

Loma Linda University Electronic Theses, Dissertations & Projects

Postural instability is one of the most debilitating symptoms of Parkinson’s disease and the best clinical prognostic indicator of progressive disease. Significant differences in neuropathology, neurochemistry, response to L-dopa therapy and stereotactic surgery as well as prognosis have been identified in subtypes when patients with predominant postural instability and gait difficulty (PIGD)/Type B were differentiated from those with predominant symptoms of tremor and rigidity/Type A. Postural instability is resistant to the therapeutic effects of L-dopa, despite its continued efficacy on other Parkinson’s symptomatology, implicating the nondopaminergic mechanism of postural instability in Parkinson’s disease. Patients with significant postural instability and gait …

Parkinsonism: Neurological Considerations, J. Dana Darnley

Henry Ford Hospital Medical Journal

No abstract provided.