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137 results on '"Bonda, David"'

3. Deep Brain Stimulation of Bilateral Centromedian Thalamic Nuclei in Pediatric Patients with Lennox-Gastaut Syndrome: An Institutional Experience

Author

Bonda, David, Kelly, Katherine A., Boop, Scott, Feroze, Abdullah H., Randle, Stephanie C., Bindschadler, Mike, Marashly, Ahmad, Owens, James, Lockrow, Jason, Bozarth, Xiuhua, Novotny, Edward, Friedman, Seth, Goldstein, Hannah E., Grannan, Benjamin L., Durfy, Sharon, Ojemann, Jeffrey G., Ko, Andrew L., and Hauptman, Jason S.

Published
2024
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9. A Comparison of Clinical Outcomes for Subependymal Giant Cell Astrocytomas Treated with Laser Interstitial Thermal Therapy, Open Surgical Resection, and mTOR Inhibitors

Author

Boop, Scott, primary, Bonda, David, additional, Randle, Stephanie, additional, Leary, Sarah, additional, Vitanza, Nicholas, additional, Crotty, Erin, additional, Novotny, Edward, additional, Friedman, Seth, additional, Ellenbogen, Richard G., additional, Durfy, Sharon, additional, Goldstein, Hannah, additional, Ojemann, Jeffrey G., additional, and Hauptman, Jason S., additional

Published
2023
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14. Response.

Author

Nisson, Peyton L., Francis, John, Michel, Michelot, and Bonda, David

Published
2025
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21. Large Adult Spinal Diffuse Midline Histone H3 Lysine27-to-Methionine-Mutant Glioma With Intramedullary and Extramedullary Components Presenting With Progressive Hydrocephalus: A Case Report Highlighting Unique Imaging Findings and Treatment

Author

Einstein, Evan H, primary, Bonda, David, additional, Hosseini, Hossein, additional, Harel, Asaff, additional, Palmer, Joshua D, additional, Giglio, Pierre, additional, Barve, Rahul, additional, Gould, Megan, additional, Lonser, Russell R., additional, and D'Amico, Randy S, additional

Published
2021
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27. Combining 3D-printing Technology with Pre-operative Sterotactic Planning for Placement of Intracranial Depth Electrodes for Improved Patient Safety and Operative Efficiency: An Institutional Experience (2558)

Author

Theroux, Liana, primary, Bonda, David J., additional, Pruitt, Rachel, additional, Goldstein, Todd, additional, Varghese, Anish, additional, Shah, Amar, additional, Rodgers, Shaun, additional, Kothare, Sanjeev, additional, and Karkare, Shefali, additional

Published
2020
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30. The pathology of Alzheimer disease elicits an in Vivo immunological response

Author

Bonda, David J., Webber, Kate M., Siedlak, Sandra L., Perry, George, Friedland, Robert P., and Smith, Mark A.

Subjects
Antibodies -- Physiological aspects, Antibodies -- Health aspects, Viral antibodies -- Physiological aspects, Viral antibodies -- Health aspects, Alzheimer's disease -- Physiological aspects, Alzheimer's disease -- Development and progression, Hippocampus (Brain) -- Chemical properties, Amyloidosis -- Physiological aspects, Blood-brain barrier -- Chemical properties, Blood-brain barrier -- Health aspects, Immunology -- Research, Pathology -- Research, Biological sciences
Abstract

Abstract: The mechanism(s) responsible for the loss of neurons that characterizes Alzheimer disease is incompletely understood. Nonetheless, there is considerable evidence suggestive of immune abnormalities coupled to alterations in blood-brain [...]

Published
2007

35. Review: Cell cycle aberrations and neurodegeneration

Author

Bonda, David J., Bonda, David J., Bajić, Vladan, Potparević, Biljana, Casadesus, G., Zhu, Xiongwei, Smith, Mark A., Lee, Hyoung-Gon, Bonda, David J., Bonda, David J., Bajić, Vladan, Potparević, Biljana, Casadesus, G., Zhu, Xiongwei, Smith, Mark A., and Lee, Hyoung-Gon

Abstract

The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re-entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re-entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a 'Two-Hit Hypothesis' that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.

Published
2010

37. The Critical Role of the Sirtuin Pathway in Aging and Alzheimer Disease: Mechanistic and Therapeutic Considerations

Author

Bonda, David J., Lee, Hyoung-gon, Camins, Antoni, Pallàs, Mercè, Casadesus, Gemma, Smith, Mark A., and Zhu, Xiongwei

Subjects
Aging, Sirtuin 1, Alzheimer Disease, Animals, Humans, Sirtuins, Article, Signal Transduction
Abstract

Advances in gerontology have yielded crucial insights into the molecular and biochemical aspects of the ageing process. The sirtuin pathway, which is most notable for its association with the anti-ageing effects of calorie restriction, has received particular attention, and pharmacological or transgenic upregulation of the sirtuin pathway has shown promising results in laboratory models of ageing. Alzheimer's disease is a neurodegenerative disease that is imposing an increasing burden on society, and is the leading cause of senile dementia worldwide. The lack of therapies for Alzheimer's disease provides a strong incentive for the development of an effective treatment strategy and, interestingly, research has uncovered a mechanism of action of the sirtuin pathway that might have therapeutic potential for Alzheimer's disease.SIRT1, one of the seven mammalian proteins of the sirtuin family of NAD(+)-dependent deacetylases, has recently been shown to attenuate amyloidogenic processing of amyloid-β protein precursor (APP) in cell culture studies in vitro and in transgenic mouse models of Alzheimer's disease. Mechanistically, SIRT1 increases α-secretase production and activity through activation of the α-secretase gene ADAM10. Because α-secretase is the enzyme responsible for the non-amyloidogenic cleavage of APP, upregulation of α-secretase shifts APP processing to reduce the pathological accumulation of the presumptive toxic Aβ species that results from β-secretase and γ-secretase activity. Interestingly, the spatial patterns of Aβ deposition in the brain might correlate with increased aerobic glycolysis in those regions. Because aerobic glycolysis depletes cellular levels of NAD(+) (through a decreased NAD(+)/NADH ratio), it is possible that a corresponding downregulation of the NAD(+)-dependent sirtuin pathway contributes to the amyloidogenic processing of APP. WHERE NEXT?: The specific inhibition of Aβ generation by SIRT1 coupled with the potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtuin pathway has translational implications. On the one hand, the possible underlying role of the sirtuin pathway in Alzheimer's disease onset and development might increase our understanding of this devastating condition. On the other hand, therapeutic upregulation of SIRT1 might provide opportunities for the amelioration of Alzheimer's-disease-type neuropathology through inhibition of amyloidogenesis. Ultimately, further analysis into both aspects is necessary if any progress is to be made.

Published
2011

39. The X-chromosome instability phenotype in Alzheimer's disease: A clinical sign of accelerating aging?

Author

Bajić, Vladan, Bajić, Vladan, Potparević, Biljana, Živković, Lada, Bonda, David J., Siedlak, Sandra L., Casadesus, Gemma, Lee, Hyoung-Gon, Smith, Mark A., Bajić, Vladan, Bajić, Vladan, Potparević, Biljana, Živković, Lada, Bonda, David J., Siedlak, Sandra L., Casadesus, Gemma, Lee, Hyoung-Gon, and Smith, Mark A.

Abstract

Premature centromere division, or premature centromere separation (PCS), occurs when chromatid separation is dysfunctional, occurring earlier than usual during the interphase stage of mitosis. This phenomenon, seen in Robert's syndrome and various cancers, has also been documented in peripheral as well as neuronal cells of Alzheimer's disease (AD). In the latter instances, fluorescent in situ hybridization (FISH), applied to the centromere region of the X-chromosome in interphase nuclei of lymphocytes from peripheral blood in AD patients, demonstrated premature chromosomal separation before mitotic metaphase directly after completion of DNA replication in G(2) phase of the cell cycle. Furthermore, and perhaps unexpectedly given the presumptive post-mitotic status of terminally differentiated neurons, neurons in AD patients also showed significantly increased levels of PCS of the X-chromosome. Taken together with other phenomena such as cell cycle re-activation and ectopic re-expression of cyclins and cyclin dependent proteins, we propose that AD is an oncogenic phenotype leading to accelarated aging of the affected brain.

Published
2009

44. Indoleamine 2,3-dioxygenase and 3-hydroxykynurenine modifications are found in the neuropathology of Alzheimer's disease

Author

Bonda, David J., primary, Mailankot, Maneesh, additional, Stone, Jeremy G., additional, Garrett, Matthew R., additional, Staniszewska, Magdalena, additional, Castellani, Rudy J., additional, Siedlak, Sandra L., additional, Zhu, Xiongwei, additional, Lee, Hyoung-gon, additional, Perry, George, additional, Nagaraj, Ram H., additional, and Smith, Mark A., additional

Published
2010
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