Current Search: Alzheimer's disease. (x)
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- Title
- Basic knowledge of Alzheimer’s disease in rural populations.
- Creator
- Wiese, Lisa Kirk, Williams, Christine L., Tappen, Ruth M., Graduate College
- Date Issued
- 2013-04-12
- PURL
- http://purl.flvc.org/fcla/dt/3361371
- Subject Headings
- Alzheimer's disease, Rural population
- Format
- Document (PDF)
- Title
- DISCOVERY OF GENES AND MOLECULAR PROCESSES THAT ARE IMPORTANT FOR THE PATHOGENESIS OF ALZHEIMER’S DISEASE.
- Creator
- Kwakye, Alexander, Li, Zhongwei, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
- Abstract/Description
-
Alzheimer’s Disease (AD) is a complex brain disorder that affects at least one in every ten persons aged 65 and above worldwide. The pathogenesis of this disorder remains elusive. In this work, we utilized a rich set of publicly available gene expression data to elucidate the genes and molecular processes that may underlie its pathogenesis. We developed a new ranking score to prioritize molecular pathways enriched in differentially expressed genes during AD. After applying our new ranking...
Show moreAlzheimer’s Disease (AD) is a complex brain disorder that affects at least one in every ten persons aged 65 and above worldwide. The pathogenesis of this disorder remains elusive. In this work, we utilized a rich set of publicly available gene expression data to elucidate the genes and molecular processes that may underlie its pathogenesis. We developed a new ranking score to prioritize molecular pathways enriched in differentially expressed genes during AD. After applying our new ranking score, GO categories such as cotranslational protein targeting to membrane, SRP-dependent cotranslational protein targeting to membrane, and spliceosomal snRNP assembly were found to be significantly associated with AD. We also confirm the protein-protein interaction between APP, NPAS4 and ARNT2 and explain that this interaction could be implicated in AD. This interaction could serve as a theoretical framework for further analyses into the role of NPAS4 and other immediate-early genes in AD pathogenesis.
Show less - Date Issued
- 2020
- PURL
- http://purl.flvc.org/fau/fd/FA00013541
- Subject Headings
- Alzheimer's disease, Alzheimer's disease--Genetic aspects, Alzheimer's disease--Molecular aspects, Alzheimer's disease--Pathogenesis
- Format
- Document (PDF)
- Title
- MULTIVALENT PROTEIN GLYCOSYLATION: A DRIVING FORCE OF CANCER PROGRESSION AND ALZHEIMER’S DISEASE PATHOGENESIS.
- Creator
- Singh, YashoNandini, Cudic, Maré, Florida Atlantic University, Department of Chemistry and Biochemistry, Charles E. Schmidt College of Science
- Abstract/Description
-
Glycosylation is a frequent and heterogeneous post-translational protein modification occurring in all domains of life. Aberrant cell-surface glycosylation is shown to mediate several processes involved in tumor cell proliferation, adhesion, and metastasis. Recent findings linked altered protein glycosylation to Alzheimer’s disease (AD) pathogenesis. One key obstacle in studying functional consequences of glycosylation has been the lack of structurally defined glycopeptide or protein model...
Show moreGlycosylation is a frequent and heterogeneous post-translational protein modification occurring in all domains of life. Aberrant cell-surface glycosylation is shown to mediate several processes involved in tumor cell proliferation, adhesion, and metastasis. Recent findings linked altered protein glycosylation to Alzheimer’s disease (AD) pathogenesis. One key obstacle in studying functional consequences of glycosylation has been the lack of structurally defined glycopeptide or protein model compounds for biochemical studies at the molecular level. For tumor progression, studies are crucial towards understanding the glycan-lectin recognition process tied to deciphering the information contained in glycan structures and for AD, foundational studies are necessary for understanding the role of O-glycosylation in protein processing and its fate toward the amyloid pathway. In chapter 1, a highly O-glycosylated transmembrane and cancer-associated mucin protein, MUC1, is used as a model for designing synthetic tools for exploring its role in metastasis via association with lectins and specificity of anti-MUC1 antibodies. This dissertation for the first time presents a MUC1-based positional scanning synthetic glycopeptide combinatorial library that varies in the number and location of tumor-associated Tn antigen. The importance of defined structural complexity for evaluating glycan density and glycosylation patterns for binding to Tn-specific plant lectins and anti-MUC1 (mouse) monoclonal antibodies was revealed using an enzyme-linked lectin assay (ELLA). Chapter 2 addressed the growing significance of peptide lectinomimics for recognizing tumor-specific glycans. Fluorescently labelled alanine scan analogues of odorranalectin (OL), a cyclic peptide that exhibits lectin like properties, were screened for binding BSA-conjugated monosaccharides using ELLA. Results revealed that Lys5, Phe7, Tyr9, Gly12, Leu14, and Thr17 were crucial for binding BSA-L-fucose, BSA-Dgalactose and BSA-N-acetyl-D-galactosamine. The thermodynamics of binding of the selected alanine analogues was evaluated by isothermal titration calorimetry. The thermodynamic profile of interactions with asialofetuin exhibits shift to an entropy-driven mechanism compared to fucoidan, which displayed an enthalpy-entropy compensation, typically associated with the carbohydrate-lectin recognition process. Chapter 3 focused on amyloid-precursor protein (APP) O-glycosylation and its role in AD pathogenesis. We synthesized native and Swedish-mutated (glyco)peptides with O-GalNAc moiety on Thr663 and/or Ser667 or Tyr681 to explore the role of glycosylation on conformation, secretase activity, and aggregation kinetics of Aβ40. Our results show that conformation is strongly dependent on external conditions such as buffer ions and solvent polarity as well as internal modifications of (glyco)peptides such as length, O-glycosylation, and Swedish mutation (Lys670Asn/Met671Leu). Furthermore, the level of β-secretase activity significantly increased for the glycopeptides containing the Swedish mutation compared to their nonglycosylated and native counterparts. Lastly, glycopeptides impacted the kinetics of Aβ40 aggregation by significantly increasing the lag phase and delaying aggregation onset, however, this effect was less pronounced for its Swedish-mutated counterparts.
Show less - Date Issued
- 2022
- PURL
- http://purl.flvc.org/fau/fd/FA00013949
- Subject Headings
- Glycosylation, Alzheimer Disease, Lectins
- Format
- Document (PDF)
- Title
- Voices of couples affected by Alzheimer's disease.
- Creator
- Bonorandi, Andrea, Williams, Christine L.
- Date Issued
- 2013-04-05
- PURL
- http://purl.flvc.org/fcla/dt/3361072
- Subject Headings
- Alzheimer's disease, Alzheimer's disease--Family relationships, Communication
- Format
- Document (PDF)
- Title
- Family resiliency, social support and validation to determine the quality of life in caregivers and persons with Alzheimer's disease.
- Creator
- Shroff, Havovi B., Frain, Michael, Graduate College
- Date Issued
- 2013-04-12
- PURL
- http://purl.flvc.org/fcla/dt/3361956
- Subject Headings
- Alzheimer's disease, Alzheimer's disease--Patients--Care, Resilience, Psychological
- Format
- Document (PDF)
- Title
- CHARACTERIZATION OF DIFFERENTIATED HUMAN NEUROBLASTOMA SH-SY5Y CELLS IN CULTURE.
- Creator
- Condikey, Siri, Prentice, Howard, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
- Abstract/Description
-
Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases affecting an estimated 20 million worldwide. The primary pathology of AD is the progressive loss of basal forebrain cholinergic neurons, which is responsible for the cognitive decline experienced by AD patients. The mechanisms underlying this selective vulnerability have not been fully elucidated. Furthermore, oxidative stress is a key factor behind the pathology of AD leading to this neuronal loss. The current...
Show moreAlzheimer’s disease (AD) is one of the most common neurodegenerative diseases affecting an estimated 20 million worldwide. The primary pathology of AD is the progressive loss of basal forebrain cholinergic neurons, which is responsible for the cognitive decline experienced by AD patients. The mechanisms underlying this selective vulnerability have not been fully elucidated. Furthermore, oxidative stress is a key factor behind the pathology of AD leading to this neuronal loss. The current literature suggests that there are limited in-vitro models available to accurately simulate the hallmark symptoms of Alzheimer's disease (AD). The SH-SY5Y cell line has been used extensively to study neuronal stress responses but the undifferentiated cell type has been predominantly used. Undifferentiated SH-SY5Y versus differentiated SH-SY5Y have been shown to have different interaction, expression and localization with AD hallmark, amyloid-b -42. This project sought to use differentiated cholinergic cells from the line SH-SY5Y to further isolate and elucidate, in-vitro, the mechanisms behind the oxidative stress response, a key stressor in the pathology of AD. Building upon previous studies, a protocol to differentiate SH-SY5Y cells with retinoic acid (RA) and neurotrophin (BDNF) to mature neurons of the cholinergic phenotype was optimized and implemented. The results showed successful differentiation into the cholinergic phenotype as evidenced via immunofluorescence imaging of choline acetyl transferase (ChAT) expression and mature neurite morphology. To simulate oxidative stress, we exposed both undifferentiated and differentiated SH-SY5Y cells to hypoxic conditions. Results indicated a stress response to mild hypoxic conditions with higher sensitivity in cholinergic differentiated SH-SY5Y. Understanding these hallmark mechanisms behind oxidative stress is crucial to developing mechanism-based therapeutics for AD.
Show less - Date Issued
- 2023
- PURL
- http://purl.flvc.org/fau/fd/FA00014347
- Subject Headings
- Alzheimer Disease, Cholinergic Neurons, Alzheimer Disease--pathology
- Format
- Document (PDF)
- Title
- MULTIMODAL THERAPIES FOR ALZHEIMER’S DISEASE.
- Creator
- Bhandari, Subash, Wu, Jang-Yen, Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
- Abstract/Description
-
Alzheimer's disease (AD) is projected to triple by 2050, highlighting the urgent need for disease-modifying treatment strategies. Our gene therapy approach tackles three critical challenges: a) delivering drugs effectively to the brain and brain bioavailability of those delivered drugs, b) intervening early in the disease process to prevent progression into nonreversible stages, and c) managing the behavioral and psychological symptoms of dementia (BPSD) that significantly impact patients and...
Show moreAlzheimer's disease (AD) is projected to triple by 2050, highlighting the urgent need for disease-modifying treatment strategies. Our gene therapy approach tackles three critical challenges: a) delivering drugs effectively to the brain and brain bioavailability of those delivered drugs, b) intervening early in the disease process to prevent progression into nonreversible stages, and c) managing the behavioral and psychological symptoms of dementia (BPSD) that significantly impact patients and caregivers. Our non-invasive ocular delivery system effectively delivered therapies to CNS as indicated by the localization of those transcribed genes and translated protein products in different brain regions, including the hippocampus, cortex, dorsal lateral geniculate nucleus, red nucleus, and pontine nucleus This approach could overcome the limitations of traditional drug delivery methods for neurological diseases. In a 3xTg AD mouse model of AD, we evaluated the efficacy of Choline Acetyltransferase (ChAT) gene therapy on early disease progression. A single treatment improved impaired memory functions such as cognitive flexibility, memory extinction and working memory, reduced amyloid beta oligomers and phosphorylated tau protein levels, and enhanced mitochondrial dynamics through the regulation of fusion, fission and mitophagy. Additionally, ChAT gene therapy modulated apoptosis, inflammation and the activity of microglia and astrocytes in parts through the activation of AKT. These findings suggest ChAT gene therapy's potential to slow or prevent AD progression if administered early in the disease course.
Show less - Date Issued
- 2024
- PURL
- http://purl.flvc.org/fau/fd/FA00014400
- Subject Headings
- Alzheimer's disease, Alzheimer's Disease--therapy, Gene therapy
- Format
- Document (PDF)
- Title
- COGNITIVE MARKERS OF PROGRESSION FROM NORMAL COGNITION TO MCI AND FROM MCI TO DEMENTIA ACROSS EUROPEAN AND HISPANIC AMERICANS.
- Creator
- Arruda, Fernanda Ponce de Leon, Rosselli, Monica, Florida Atlantic University, Department of Psychology, Charles E. Schmidt College of Science
- Abstract/Description
-
Objective: Our main objectives were to identify cognitive markers of progression to a more severe cognitive diagnosis, explore possible differences between ethnic groups and to correlate cognitive markers of progression with biomarkers of AD (hippocampal and entorhinal volumes) and frontal volumes (lateral orbitofrontal, medial orbitofrontal, superior frontal, and rostral middle frontal volumes). Method: 207 participants (Mage = 71.79, SD = 7.48, 123 Hispanic Americans [HA]) were followed for...
Show moreObjective: Our main objectives were to identify cognitive markers of progression to a more severe cognitive diagnosis, explore possible differences between ethnic groups and to correlate cognitive markers of progression with biomarkers of AD (hippocampal and entorhinal volumes) and frontal volumes (lateral orbitofrontal, medial orbitofrontal, superior frontal, and rostral middle frontal volumes). Method: 207 participants (Mage = 71.79, SD = 7.48, 123 Hispanic Americans [HA]) were followed for an average of 23 months. Participants were classified into 3 diagnostic groups (Cognitively normal [CN], mild cognitive impairment [MCI], or dementia) based on the CDR global score and the neuropsychological baseline data was used as predictors of progression status. For the CN group, the Benson Figure delayed recall was a predictor of cognitive decline, and within the MCI group, the Benson delayed recall, the HVLT immediate recall, the TMTB, category fluency, and three measures of the LASSI-L (A1 cued recall, A2 cued recall, and delayed recall) were significant predictors of progression to dementia and are suggested as cognitive markers of progression for MCI individuals. Memory cognitive markers and category fluency correlated with medial temporal lobe volumes, and the TMT-B correlated with superior frontal volume. We did not observe significant differences in cognitive markers across ethnic groups. Conclusion: we identified cognitive markers of progression for CN and for MCI diagnoses which were not different across ethnic groups. These findings contribute to literature on the early identification of individuals at risk of progression to a more severe cognitive status even within asymptomatic individuals which can facilitate a more time- and cost-effective practice that is essential to the provision of the appropriate treatment to those at higher risk of progression.
Show less - Date Issued
- 2022
- PURL
- http://purl.flvc.org/fau/fd/FA00013924
- Subject Headings
- Alzheimer Disease, Biomarkers, Hispanic Americans
- Format
- Document (PDF)
- Title
- Myokine Cathepsin B Expression with Exercise Training in the 3xTg-AD Murine Model of Alzheimer’s Disease.
- Creator
- Paez, Hector G., Khamoui, Andy V., Florida Atlantic University, College of Education, Department of Exercise Science and Health Promotion
- Abstract/Description
-
This research investigated the relationship between exercise training and cathepsin B expression in the 3xTg-AD murine model of Alzheimer’s disease. 3xTg-AD mice were assigned to control (Tg, n=10), aerobic training (Tg+AT, n=10), or resistance training (Tg+RT, n=10). RotaRod peak latency and grip strength were assessed as preand post-measurements. Skeletal muscle was collected after training and analyzed for cathepsin B protein. Tg+RT showed greater grip strength than Tg and Tg+AT at...
Show moreThis research investigated the relationship between exercise training and cathepsin B expression in the 3xTg-AD murine model of Alzheimer’s disease. 3xTg-AD mice were assigned to control (Tg, n=10), aerobic training (Tg+AT, n=10), or resistance training (Tg+RT, n=10). RotaRod peak latency and grip strength were assessed as preand post-measurements. Skeletal muscle was collected after training and analyzed for cathepsin B protein. Tg+RT showed greater grip strength than Tg and Tg+AT at posttesting (p ≤ 0.05). Only Tg+AT showed an improvement in RotaRod peak latency (p ≤ 0.05). Gastrocnemius weight was greater in Tg+RT compared to Tg (p ≤ 0.05), and no differences were observed in cathepsin B or procathepsin B expression (p > 0.05). This data suggests that cathepsin B was not induced by either mode of exercise training, however, physical function and muscle mass were improved, therefore inclusion of both training modalities may address peripheral comorbidities in Alzheimer’s disease.
Show less - Date Issued
- 2018
- PURL
- http://purl.flvc.org/fau/fd/FA00013092
- Subject Headings
- Cathepsins., Alzheimer's disease., Aerobic exercises., Resistance Training.
- Format
- Document (PDF)
- Title
- STREAMLINING CLINICAL DETECTION OF ALZHEIMER’S DISEASE USING ELECTRONIC HEALTH RECORDS AND MACHINE LEARNING TECHNIQUES.
- Creator
- Kleiman, Michael J., Barenholtz, Elan, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Psychology
- Abstract/Description
-
Alzheimer’s disease is typically detected using a combination of cognitive-behavioral assessment exams and interviews of both the patient and a family member or caregiver, both administered and interpreted by a trained physician. This procedure, while standard in medical practice, can be time consuming and expensive for both the patient and the diagnostician especially because proper training is required to interpret the collected information and determine an appropriate diagnosis. The use of...
Show moreAlzheimer’s disease is typically detected using a combination of cognitive-behavioral assessment exams and interviews of both the patient and a family member or caregiver, both administered and interpreted by a trained physician. This procedure, while standard in medical practice, can be time consuming and expensive for both the patient and the diagnostician especially because proper training is required to interpret the collected information and determine an appropriate diagnosis. The use of machine learning techniques to augment diagnostic procedures has been previously examined in limited capacity but to date no research examines real-world medical applications of predictive analytics for health records and cognitive exam scores. This dissertation seeks to examine the efficacy of detecting cognitive impairment due to Alzheimer’s disease using machine learning, including multi-modal neural network architectures, with a real-world clinical dataset used to determine the accuracy and applicability of the generated models. An in-depth analysis of each type of data (e.g. cognitive exams, questionnaires, demographics) as well as the cognitive domains examined (e.g. memory, attention, language) is performed to identify the most useful targets, with cognitive exams and questionnaires being found to be the most useful features and short-term memory, attention, and language found to be the most important cognitive domains. In an effort to reduce medical costs and streamline procedures, optimally predictive and efficient groups of features were identified and selected, with the best performing and economical group containing only three questions and one cognitive exam component, producing an accuracy of 85%. The most effective diagnostic scoring procedure was examined, with simple threshold counting based on medical documentation being identified as the most useful. Overall predictive analysis found that Alzheimer’s disease can be detected most accurately using a bimodal multi-input neural network model using separated cognitive domains and questionnaires, with a detection accuracy of 88% using the real-world testing set, and that the technique of analyzing domains separately serves to significantly improve model efficacy compared to models that combine them.
Show less - Date Issued
- 2019
- PURL
- http://purl.flvc.org/fau/fd/FA00013326
- Subject Headings
- Alzheimer's disease, Electronic Health Records, Machine learning
- Format
- Document (PDF)
- Title
- Role of the N-Terminal Hydrophilic Region of Amyloid Beta Peptide in Amyloidogenesis, Membrane Interaction and Toxicity Associated with Alzheimer’s Disease.
- Creator
- Morris, Clifford M., Du, Deguo, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Chemistry and Biochemistry
- Abstract/Description
-
Alzheimer’s disease (AD) is a deleterious neurodegenerative disease caused in major part by the aberrant processing and accumulation of amyloid beta peptides. In this dissertation, we systematically investigated the role of N-terminal region (NTR) residues of amyloid (1-40) (Aβ40) peptide in amyloidogenesis, lipid bilayer membrane interaction and damage, as well as neurotoxicity. Herein, we investigated the role of NTR residues on the aggregation and amyloid fibril formation process, to gain...
Show moreAlzheimer’s disease (AD) is a deleterious neurodegenerative disease caused in major part by the aberrant processing and accumulation of amyloid beta peptides. In this dissertation, we systematically investigated the role of N-terminal region (NTR) residues of amyloid (1-40) (Aβ40) peptide in amyloidogenesis, lipid bilayer membrane interaction and damage, as well as neurotoxicity. Herein, we investigated the role of NTR residues on the aggregation and amyloid fibril formation process, to gain understanding on the electrostatic and hydrophobic constituents of the mechanism. This was achieved by substituting specific charged residues located in the NTR of Aβ40 and investigating their effects through a variety of techniques. We also investigated the role of NTR charged residues in their interaction with supported phospholipid bilayer membranes through the use of Quartz Crystal Microbalance with Dissipation (QCM-D) monitoring to gain insight on the mechanistic details of the interaction. To further understand the implications of substituting charged NTR residues on membrane interaction, pore formation and damage, we utilized a carboxyfluorescein dye leakage assay to quantify the membrane damage caused by Aβ40 and the NTR mutants. We also performed neurotoxicity assay with SH-SY5Y neuroblastoma cells to shed light on the effects of NTR substitutions on cellular toxicity. Finally, we synthesized a polymer, trimethyl chitosan (TMC), and utilized it as a polyelectrolyte monitor of electrostatic interactions occurring between TMC and the NTR of Aβ40. Our results demonstrate that the NTR charged residues of Aβ40 contribute significantly to the aggregation process, amyloidogenesis, and phospholipid membrane interaction and perturbation by means of electrostatic, thermodynamic and hydrophobic forces.
Show less - Date Issued
- 2019
- PURL
- http://purl.flvc.org/fau/fd/FA00013246
- Subject Headings
- Alzheimer's disease, Amyloid beta-Peptides, Amyloid
- Format
- Document (PDF)
- Title
- Verbal fluency in bilingual Alzheimer's disease patients.
- Creator
- Salvatierra, Judy Lee, Florida Atlantic University, Rosselli, Monica
- Abstract/Description
-
Studies have demonstrated that in verbal fluency tests monolingual AD patients show greater difficulties retrieving words under semantic conditions compared to phonemic. This study tried to determine whether this was reproduced in both languages of Spanish/English bilingual AD patients. Performance on verbal fluency was also compared to AD severity. A difference in performance was found based on language and on cue condition. An interaction between AD severity and cue condition was also found...
Show moreStudies have demonstrated that in verbal fluency tests monolingual AD patients show greater difficulties retrieving words under semantic conditions compared to phonemic. This study tried to determine whether this was reproduced in both languages of Spanish/English bilingual AD patients. Performance on verbal fluency was also compared to AD severity. A difference in performance was found based on language and on cue condition. An interaction between AD severity and cue condition was also found. Patients that were categorized as less severe produced more words under the semantic condition while those that were categorized as more severe did not show a difference between conditions suggesting a faster decline in semantic verbal fluency tests. Furthermore, this pattern was produced in both languages.
Show less - Date Issued
- 2003
- PURL
- http://purl.flvc.org/fcla/dt/13085
- Subject Headings
- Alzheimer's disease--Patients, Speech disorders
- Format
- Document (PDF)
- Title
- Studying the Effects of Lipid Membranes and Polysaccharides on the Amyloidogenicity of Fragments of Amyloid Beta.
- Creator
- Petersen, Katherine, Du, Deguo, Florida Atlantic University, Department of Chemistry and Biochemistry, Charles E. Schmidt College of Science
- Abstract/Description
-
The amyloid beta (Aβ) peptide has been linked to Alzheimer’s Disease (AD) since the early 1990s. Since then, many studies have characterized the peptide and examined its aggregation process. Aβ is a 40 or 42-residue peptide, composed of a charged N-terminal and hydrophobic C-terminal, that aggregates into characteristic β-sheets forming insoluble plaques in the brains of (AD) patients. In recent years an intermediate oligomeric species has been shown to interact with lipid membranes, largely...
Show moreThe amyloid beta (Aβ) peptide has been linked to Alzheimer’s Disease (AD) since the early 1990s. Since then, many studies have characterized the peptide and examined its aggregation process. Aβ is a 40 or 42-residue peptide, composed of a charged N-terminal and hydrophobic C-terminal, that aggregates into characteristic β-sheets forming insoluble plaques in the brains of (AD) patients. In recent years an intermediate oligomeric species has been shown to interact with lipid membranes, largely resulting in the etiology of AD. In this study, two fragments are used, the 23-residue N-terminal fragment, Aβ23 and the 30-residue C-terminal fragment, Aβ11-40, to better understand the role of the N and C-terminus in the aggregation of Aβ peptide. Aβ11-40 has also been found in the brains of AD patients, playing a biological role in the disease. This study used analytical and biophysical techniques to systematically synthesize, purify, characterize, and study these fragments' aggregation in different conditions. We investigated the effects of lipid membranes on the aggregation of Aβ23 and Aβ11-40 and the activities of these peptides in inducing membrane damage. The results show that the aggregation of Aβ23 was increased in the presence of lipid membranes, likely due to favorable electrostatic interactions. However, the aggregation of Aβ11-40 was not influenced by lipid membranes. A dye leakage study was carried out to study the membrane damage occurring as a result of fragments' interaction with lipid membranes. The results showed that neither fragment had a profound effect on membrane destruction, although the charge of the lipid head seemed to play a role. This work's second study focused on the effect of three specific polysaccharides, heparin, chitosan (CHT), and trimethyl chitosan (TMC), on the aggregation of Aβ23 and Aβ11-40. The results showed that for Aβ23, heparin increased aggregation, while both CHT and TMC decreased aggregation. However, for Aβ11-40, both heparin and CHT did not affect aggregation, while TMC decreased aggregation.
Show less - Date Issued
- 2023
- PURL
- http://purl.flvc.org/fau/fd/FA00014294
- Subject Headings
- Amyloid beta-Peptides, Alzheimer's disease
- Format
- Document (PDF)
- Title
- THE RELATIONSHIP BETWEEN STIGMA AND LEVEL OF ALZHEIMER'S DISEASE KNOWLEDGE WITHIN THE SAUDI CULTURE.
- Creator
- Jambi, Amnah, Butcher, Howard K., Florida Atlantic University, Christine E. Lynn College of Nursing, Christine E. Lynn College of Nursing
- Abstract/Description
-
There are two types of stigmas: self-stigma and public stigma. The focus of this dissertation was public stigma. The public stigma encountered by persons with Alzheimer’s Disease (AD) contributes to the isolation of families due to the effort made by AD caregivers to adjust to social challenges (Abojabel & Warner, 2019). According to the Saudi Alzheimer’s Disease Association (2022), there are 130 thousand documented cases of AD, which comprised 9% of the aged population. The severity of...
Show moreThere are two types of stigmas: self-stigma and public stigma. The focus of this dissertation was public stigma. The public stigma encountered by persons with Alzheimer’s Disease (AD) contributes to the isolation of families due to the effort made by AD caregivers to adjust to social challenges (Abojabel & Warner, 2019). According to the Saudi Alzheimer’s Disease Association (2022), there are 130 thousand documented cases of AD, which comprised 9% of the aged population. The severity of stigmas can vary across cultures because stigmas of disease are connected to cultural norms (Corrigan, 2014). Most studies conducted in Saudi Arabia have assessed public stigma regarding mental illnesses, but no study has been found regarding public stigma within the AD scope. Population-based approaches that attempt to clarify stigma level prevalence in representative samples are important to develop methods to address these disparities and ensure equitable access to health care within the population's cultural context. The aim of this study was to 1) identify the relationship between public stigma and the level of AD knowledge among the Saudi population and 2) identify the potential factors that were associated with public stigma and AD knowledge levels among Saudi community members, within the context of a caring science perspective using critical caring theory and specific-situation theory.
Show less - Date Issued
- 2023
- PURL
- http://purl.flvc.org/fau/fd/FA00014320
- Subject Headings
- Alzheimer Disease, Saudi Arabia, Stigma (Social psychology)
- Format
- Document (PDF)
- Title
- DISSECTING THE MECHANISTIC ROLES OF REGULATORS IN MEDIATING AMYLOID-BETA AMYLOIDOGENESIS.
- Creator
- Shen, Fengyun, Du, Deguo, Florida Atlantic University, Department of Chemistry and Biochemistry, Charles E. Schmidt College of Science
- Abstract/Description
-
Alzheimer’s disease (AD) is a common neurodegenerative disorder. The most recognized disease pathology is the Amyloid-β (Aβ) cascade hypothesis which states that the accumulation of Aβ plaques might be the cause of AD. In the AD brain, Aβ plaques stockpile a variety of molecular components including metals, lipids, nucleic acids, carbohydrates, and peptides, indicating Aβ aggregation might be influenced by these modulators. In this dissertation, we investigated the effects of Zn2+ and...
Show moreAlzheimer’s disease (AD) is a common neurodegenerative disorder. The most recognized disease pathology is the Amyloid-β (Aβ) cascade hypothesis which states that the accumulation of Aβ plaques might be the cause of AD. In the AD brain, Aβ plaques stockpile a variety of molecular components including metals, lipids, nucleic acids, carbohydrates, and peptides, indicating Aβ aggregation might be influenced by these modulators. In this dissertation, we investigated the effects of Zn2+ and carnosine, phospholipids, and β-hairpins on Aβ aggregation to dissect their mechanistic roles in the amyloidogenesis of Aβ. We first systematically studied the kinetic impact of Zn2+ on the aggregation of Aβ40 and Aβ40-M. Our results show that the presence of Zn2+ transforms the Aβ40 aggregation kinetics from a single sigmoidal to a biphasic process, while the aggregation of Aβ40-M is significantly suppressed by Zn2+. We also found that a nature dipeptide, carnosine, remarkably decreases the activity of Zn2+ on modulating Aβ aggregation, although it has a weak direct effect on the peptide aggregation kinetics. Second, we investigated the activities of Aβ40 and Aβ42 in inducing membrane damage and the effects of lipid membranes on the aggregation of these peptides using liposome models containing mitochondrial-specific phospholipid–cardiolipin (CL).
Show less - Date Issued
- 2023
- PURL
- http://purl.flvc.org/fau/fd/FA00014314
- Subject Headings
- Alzheimer's disease, Amyloid beta-Peptides, Neurodegenerative Diseases
- Format
- Document (PDF)
- Title
- White matter networks indicative of Alzheimer's disease from diffusion MRI.
- Creator
- Hahn, William E., Fuchs, Armin, Graduate College
- Date Issued
- 2013-04-12
- PURL
- http://purl.flvc.org/fcla/dt/3361307
- Subject Headings
- Alzheimer's disease, Diffusion tensor imaging, Diffusion magnetic resonance imaging
- Format
- Document (PDF)
- Title
- Amyloid Cascade Hypothesis Perspective on Alzheimer's Disease.
- Creator
- Elsouri, Kawther, Kantorow, Marc, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
- Abstract/Description
-
Alzheimer’s disease (AD) has been defined as a type of dementia that causes problems with memory, thinking, and behavior. AD is characterized by tau tangles and Aβ plaques in and around neurons, respectively. The impact this disease has on its victims’ health, both physically and mentally, is unimaginable and the rate of progression is not expected to decrease any time soon. This threat to our minds encourages the importance of understanding AD. Amongst the theories as to what bio mechanisms...
Show moreAlzheimer’s disease (AD) has been defined as a type of dementia that causes problems with memory, thinking, and behavior. AD is characterized by tau tangles and Aβ plaques in and around neurons, respectively. The impact this disease has on its victims’ health, both physically and mentally, is unimaginable and the rate of progression is not expected to decrease any time soon. This threat to our minds encourages the importance of understanding AD. Amongst the theories as to what bio mechanisms cause the brain to intertwine is the amyloid cascade hypothesis. The purpose of this thesis is to review the amyloid cascade hypothesis and discuss treatments which utilize this model. We also wish to examine social aspects such as loneliness and socioeconomic factors which are associated with the progression of AD. Research presented provides evidence that targeting the accumulation of Aβ in the brain will prevent further biochemical responses to form neurodegenerative pathology. From the collected data, we observe that therapies targeting the amyloidogenic pathway have received positive feedback in the medical community. Amongst them, an Aβ synthetic peptide vaccine which made history in vaccine development due to their responder rate. The impact of social factors such as loneliness in the advancement of AD is also supported by research. While it is acknowledged that any neurodegenerative disease is far too complex to narrow its cause specifically, this thesis provides an association with multiple aspects that can be understood and applied to future research in this field.
Show less - Date Issued
- 2018
- PURL
- http://purl.flvc.org/fau/fd/FA00005986
- Subject Headings
- Alzheimer Disease--etiology, Amyloid, Amyloid beta-protein
- Format
- Document (PDF)
- Title
- Aggregation kinetics of A\U+fffd\ peptides and the inhibition effects of small molecules on A\U+fffd\ peptide aggregation.
- Creator
- Hijazi, Ahmad Alex., Charles E. Schmidt College of Science, Department of Chemistry and Biochemistry
- Abstract/Description
-
The pathology of Alzheimer's disease (AD) remains elusive. Competing evidence links amylois \U+fffd\-peptide (A\U+fffd\) amyloid formation to the phenotype of AD (1). The mechanism of amyloid fibril formation has been an ongoing investigation for many years. A\U+fffd\10-23 peptide, a fragment of A\U+fffd\1-42 peptide, contained crucial hydrophobic core residues (2). In this study, an investigation was launched to study the aggreagation process of A\U+fffd\1023 peptide and its ability to form...
Show moreThe pathology of Alzheimer's disease (AD) remains elusive. Competing evidence links amylois \U+fffd\-peptide (A\U+fffd\) amyloid formation to the phenotype of AD (1). The mechanism of amyloid fibril formation has been an ongoing investigation for many years. A\U+fffd\10-23 peptide, a fragment of A\U+fffd\1-42 peptide, contained crucial hydrophobic core residues (2). In this study, an investigation was launched to study the aggreagation process of A\U+fffd\1023 peptide and its ability to form amyloid fibrils. Furthermore, the presence of its hydrophobic core showed importance for its ability to aggregate and form amyloid fibrils. Thereafter, the inhibition of A\U+fffd\1-42 peptide aggregation was studied by using pyrimidine-based compounds. A\U+fffd\1-42 peptides, known to be neurotoxic, aggregate to form amyloid fibrils (3). This investigation may provide insight into the development of novel small molecular candidates to treat AD.
Show less - Date Issued
- 2012
- PURL
- http://purl.flvc.org/FAU/3358550
- Subject Headings
- Amyloid beta-protein, Proteins, Metabolism, Disorders, Prions, Alzheimer's disease
- Format
- Document (PDF)
- Title
- THERAPEUTIC STRATEGIES USING SULINDAC AND G-CSF GENE THERAPY FOR NEUROLOGICAL DISEASE.
- Creator
- Chen, Belinda, Prentice, Howard, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
- Abstract/Description
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Alzheimer’s disease is a neurodegenerative disease that causes cognitive dysfunction and leads to progressive memory loss and behavioral impairment. About 60% to 80% of dementia cases are attributed to Alzheimer’s disease and currently afflict about 50 million people worldwide. Although it primarily affects people over the age of 65, a person’s risk for developing Alzheimer’s disease earlier can depend on factors such as a family history (genetic inheritance) or experiencing an ischemic...
Show moreAlzheimer’s disease is a neurodegenerative disease that causes cognitive dysfunction and leads to progressive memory loss and behavioral impairment. About 60% to 80% of dementia cases are attributed to Alzheimer’s disease and currently afflict about 50 million people worldwide. Although it primarily affects people over the age of 65, a person’s risk for developing Alzheimer’s disease earlier can depend on factors such as a family history (genetic inheritance) or experiencing an ischemic stroke event. Current treatments for Alzheimer’s disease include behavioral therapy and drug treatment that can lessen the severity of symptoms but cannot stop progression indefinitely. Sulindac is a non-steroidal anti-inflammatory drug that, by a mechanism independent of its anti-inflammatory properties, has shown to express a preconditioning response to protect from oxidative damage. Granulocyte colony stimulating factor is a hematopoietic glycoprotein that can stimulate the production of granulocytes and stem cells that has proven to provide neuroprotection in models of ischemic stroke via mechanisms including anti-apoptosis and anti-inflammation. In this in vitro study, the potential neuroprotective effects of Sulindac is measured against the effects of oxidative stress when subjected to hypoxia and reperfusion. Regarding un-transfected SHSY-5Y cells, hypoxia was demonstrated to lower cell viability starting at a period of 12 hours. It was found that a low concentration of Sulindac (200 uM) was effective in protecting SHSY-5Y cells against oxidative stress and overall lowering the rate of cell death in the event of hypoxic and reperfusion injury. When SHSY-5Y cells were transfected with Swedish APP mutation, cell viability was also markedly decreased in hypoxic conditions. However when treated with a concentration of 600 uM of Sulindac, cell viability levels were near matched with its normoxic counterparts
Show less - Date Issued
- 2022
- PURL
- http://purl.flvc.org/fau/fd/FA00014021
- Subject Headings
- Sulindac, Granulocyte-colony stimulating factor, Genetic Therapy, Alzheimer Disease
- Format
- Document (PDF)
- Title
- Applying Story-Guided Dialogue to Examine Social Connections for Rural Caregivers of Persons Living with Alzheimer’s Disease and Related Dementias During A Global Pandemic.
- Creator
- Cappo, Kathleen, Wiese, Lisa Kirk, Florida Atlantic University, Christine E. Lynn College of Nursing, Christine E. Lynn College of Nursing
- Abstract/Description
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In the U.S., an estimated 16 million persons provide unpaid care for family and friends with Alzheimer’s disease and related dementias (ADRD). These caregivers are experiencing challenges, such as lack social interaction, which further impacts their own health. Social isolation for caregivers is now considered to be another challenge due to living in a global pandemic. The purpose of this study was to address the gap in understanding rural informal caregiver by examining social connectedness...
Show moreIn the U.S., an estimated 16 million persons provide unpaid care for family and friends with Alzheimer’s disease and related dementias (ADRD). These caregivers are experiencing challenges, such as lack social interaction, which further impacts their own health. Social isolation for caregivers is now considered to be another challenge due to living in a global pandemic. The purpose of this study was to address the gap in understanding rural informal caregiver by examining social connectedness through the use of story-guided dialogues among rural caregivers of PWD during a global pandemic. Story Theory guides intentional dialogue, to bring forward connecting with self-in-relation through use of story path, noting low, high, and turning points.
Show less - Date Issued
- 2022
- PURL
- http://purl.flvc.org/fau/fd/FA00013983
- Subject Headings
- Caregivers, Rural caregivers, Alzheimer's disease, Social isolation, Pandemics
- Format
- Document (PDF)