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Full-Text Articles in Medicine and Health Sciences

Granulins Modulate Liquid–Liquid Phase Separation And Aggregation Of The Prion-Like C-Terminal Domain Of The Neurodegeneration-Associated Protein Tdp-43, Anukool A. Bhopatkar, Vladimir N. Uversky, Vijayaraghavan Rangachari Jan 2020

Granulins Modulate Liquid–Liquid Phase Separation And Aggregation Of The Prion-Like C-Terminal Domain Of The Neurodegeneration-Associated Protein Tdp-43, Anukool A. Bhopatkar, Vladimir N. Uversky, Vijayaraghavan Rangachari

Molecular Medicine Faculty Publications

TAR DNA-binding protein 43 (TDP-43) has emerged as a key player in many neurodegenerative pathologies, including frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). Hallmarks of both FTLD and ALS are the toxic cytoplasmic inclusions of the prion-like C-terminal fragments of TDP-43 CTD (TDP-43 C-terminal domain), formed upon proteolytic cleavage of full-length TDP-43 in the nucleus and subsequent transport to the cytoplasm. Both full-length TDP-43 and its CTD are also known to form stress granules by coacervating with RNA in the cytoplasm during stress and may be involved in these pathologies. Furthermore, mutations in the PGRN gene, leading to …


Advancing Stem Cell Therapy For Repair Of Damaged Lung Microvasculature In Amyotrophic Lateral Sclerosis, Svitlana Garbuzova-Davis, Robert Shell, Hilmi Mustafa, Surafuale Hailu, Alison E. Willing, Paul R. Sanberg, Cesar V. Borlongan Jan 2020

Advancing Stem Cell Therapy For Repair Of Damaged Lung Microvasculature In Amyotrophic Lateral Sclerosis, Svitlana Garbuzova-Davis, Robert Shell, Hilmi Mustafa, Surafuale Hailu, Alison E. Willing, Paul R. Sanberg, Cesar V. Borlongan

Neurosurgery and Brain Repair Faculty Publications

Amyotrophic lateral sclerosis (ALS) is a fatal disease of motor neuron degeneration in the brain and spinal cord. Progressive paralysis of the diaphragm and other respiratory muscles leading to respiratory dysfunction and failure is the most common cause of death in ALS patients. Respiratory impairment has also been shown in animal models of ALS. Vascular pathology is another recently recognized hallmark of ALS pathogenesis. Central nervous system (CNS) capillary damage is a shared disease element in ALS rodent models and ALS patients. Microvascular impairment outside of the CNS, such as in the lungs, may occur in ALS, triggering lung damage …


Relationship Between Intelligibility And Response Accuracy Of The Amazon Echo In Individuals With Amyotrophic Lateral Sclerosis Exhibiting Mild-Moderate Dysarthria, Caroline A. Layden Jun 2018

Relationship Between Intelligibility And Response Accuracy Of The Amazon Echo In Individuals With Amyotrophic Lateral Sclerosis Exhibiting Mild-Moderate Dysarthria, Caroline A. Layden

USF Tampa Graduate Theses and Dissertations

There is an ever-growing and increasing amount of technology options that use speech recognition software. Currently, the market includes smartphones, computers, and individual smart home personal assistants that allow for hands-free access to this technology. Research studies have explored the utility of these assistive devices for the completion of activities of daily living; however, there is limited research looking at the accuracy of voice recognition software within smart home personal assistants in populations with disordered speech. In persons with amyotrophic lateral sclerosis (ALS), symptoms include changes to motor functions, speech in particular, and it is unknown how some of these …


Strategies For Preventing Age And Neurodegenerative Disease-Associated Mitochondrial Dysfunction, Vedad Delic Jan 2015

Strategies For Preventing Age And Neurodegenerative Disease-Associated Mitochondrial Dysfunction, Vedad Delic

USF Tampa Graduate Theses and Dissertations

Mitochondrial dysfunction plays a pivotal role in the development of aging phenotypes and aging-associated neurodegenerative disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS). Strategies that restore mitochondrial dysfunction may rescue the deficits of central metabolism in these disorders and improve cell survival. For example, we found that modulating the mTOR signaling pathway in a tissue culture model of aging-induced mitochondrial DNA mutation enhanced mitochondrial function as evidenced by increased oxygen consumption. Our previous melatonin studies also led us to hypothesize that caloric restriction and the hormone melatonin would reverse brain mitochondrial dysfunction in animal …