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Articles 1 - 10 of 10
Full-Text Articles in Medicine and Health Sciences
A Functional Polymorphism Within Plasminogen Activator Urokinase (Plau) Is Associated With Alzheimer's Disease, Matthias Riemenschneider, Lidija Konta, Patricia Friedrich, Sandra Schwarz, Kevin Taddei, Frauke Neff, Alessandro Padovani, Heike Kolsch, Simon Laws, Norman Klopp, Heike Bickeboller, Stefan Wagenpfeil, Jakob Mueller, Albert Rosenberger, Janine Diehl-Schmid, Silvana Archetti, Nicola Lautenschlager, Barbara Borroni, Ulrich Muller, Thomas Illig, Reinhard Heun, Rupert Egensperger, Jurgen Schlege, Hans Forstl, Ralph Martins, German Sib-Pair Study Group, Alexander Kurz
A Functional Polymorphism Within Plasminogen Activator Urokinase (Plau) Is Associated With Alzheimer's Disease, Matthias Riemenschneider, Lidija Konta, Patricia Friedrich, Sandra Schwarz, Kevin Taddei, Frauke Neff, Alessandro Padovani, Heike Kolsch, Simon Laws, Norman Klopp, Heike Bickeboller, Stefan Wagenpfeil, Jakob Mueller, Albert Rosenberger, Janine Diehl-Schmid, Silvana Archetti, Nicola Lautenschlager, Barbara Borroni, Ulrich Muller, Thomas Illig, Reinhard Heun, Rupert Egensperger, Jurgen Schlege, Hans Forstl, Ralph Martins, German Sib-Pair Study Group, Alexander Kurz
Simon Laws
A number of susceptibility loci for Alzheimer's disease (AD) have been identified including a region on Chromosome 10q21–q22. Within this region the plasminogen activator urokinase gene (PLAU) was considered as a reasonable candidate from its functional implication in plasmin generation, a serine protease capable of degrading beta-Amyloid (Aβ) protein. We screened 56 single nucleotide polymorphisms (SNPs) around PLAU using 1751 individuals from four independent case–control samples (Munich, N=679; Bonn N=282; Brescia (Italy) N=219; Perth (Australia) N=557 and one discordant sib-pair sample (Munich N=622). In brain tissue samples of neuropathologically confirmed cases with AD (N=33) we analyzed plaque counts according to …
Biophysical Understanding Of Novel Synthetic Amyloid-Β (Aβ) Prions In Alzheimer's Disease, Amit Kumar
Biophysical Understanding Of Novel Synthetic Amyloid-Β (Aβ) Prions In Alzheimer's Disease, Amit Kumar
Dissertations
Oligomers of amyloid-β (Aβ) peptide are the primary toxic agents that play a pivotal role in the pathogenesis of Alzheimer’s disease (AD). Oligomers are the intermediates formed during the Aβ aggregation process leading up to insoluble fibrils. It is important to know that oligomers can also be formed via pathways that do not lead to fibril formation. Such ‘off-pathway’ oligomers would have significantly longer half-lives than the ‘on-pathway’ ones, which may result in prolonged toxicity to neuronal cells. Furthermore, neither the mechanism of neurotoxicity nor the potential mechanisms of propagation and proliferation to neighboring cells are well understood. Moreover, recent …
How Do Older People Describe Others With Cognitive Impairment? A Multiethnic Study In The United States, Sarah B. Laditka, James N. Laditka, Rui Liu, Anna E. Price
How Do Older People Describe Others With Cognitive Impairment? A Multiethnic Study In The United States, Sarah B. Laditka, James N. Laditka, Rui Liu, Anna E. Price
All PTHMS Faculty Publications
We studied how older people describe others with cognitive impairment. Forty-two focus groups represented African Americans, American Indians, Chinese Americans, Latinos, Vietnamese Americans, and Whites other than Latinos (Whites) (N = 396, ages 50+), in nine locations in the United States of America. Axial coding connected categories and identified themes. The constant comparison method compared themes across ethnic groups. African Americans, American Indians and Whites emphasised memory loss. African Americans, American Indians, Latinos and Whites stressed withdrawal, isolation and repetitive speech. African Americans, American Indians, Vietnamese Americans and Whites emphasised ‘slow thinking’. Only Whites described mood swings and personality changes. …
Evidence-Based Guideline: Wandering, May Futrell, Karen Melillo, Ruth Remington
Evidence-Based Guideline: Wandering, May Futrell, Karen Melillo, Ruth Remington
Ruth Remington
No abstract provided.
Deficiency In P38Β Mapk Fails To Inhibit Cytokine Production Or Protect Neurons Against Inflammatory Insult In In Vitro And In Vivo Mouse Models, Bin Xing, Adam D. Bachstetter, Linda J. Van Eldik
Deficiency In P38Β Mapk Fails To Inhibit Cytokine Production Or Protect Neurons Against Inflammatory Insult In In Vitro And In Vivo Mouse Models, Bin Xing, Adam D. Bachstetter, Linda J. Van Eldik
Sanders-Brown Center on Aging Faculty Publications
The p38 MAPK pathway plays a key role in regulating the production of proinflammatory cytokines, such as TNFα and IL-1β, in peripheral inflammatory disorders. There are four major isoforms of p38 MAPK (p38α, β, δ, γ), with p38α and p38β the targets of most p38 MAPK inhibitor drugs. Our previous studies demonstrated that the p38α MAPK isoform is an important contributor to stressor-induced proinflammatory cytokine up-regulation and neurotoxicity in the brain. However, the potential role of the p38β MAPK isoform in CNS proinflammatory cytokine overproduction and neurotoxicity is poorly understood. In the current studies, we used primary microglia from wild …
Analysis Of Autophagy And Inflammasome Regulation In Neuronal Cells And Monocytes Infected With Chlamydia Pneumoniae: Implications For Alzheimer’S Disease, Brian J. Balin, Christine J. Hammond, Juliana Zoga, Ahmad B. Cader, Annette K. Slutter, Jonathan M. Anzman, Ian Kohler, Susan T. Hingley, Denah M. Appelt
Analysis Of Autophagy And Inflammasome Regulation In Neuronal Cells And Monocytes Infected With Chlamydia Pneumoniae: Implications For Alzheimer’S Disease, Brian J. Balin, Christine J. Hammond, Juliana Zoga, Ahmad B. Cader, Annette K. Slutter, Jonathan M. Anzman, Ian Kohler, Susan T. Hingley, Denah M. Appelt
Scholarly Posters
Objectives: Our laboratory has been studying the role of infection with the obligate intracellular bacterium Chlamydia pneumoniae in sporadic late-onset Alzheimer disease (LOAD). This infection may be a trigger for the pathology observed in LOAD as a function of initiating changes in gene regulation following entry of the organism into the brain. As such, we are analyzing how this infection can promote changes in autophagy and inflammasome gene regulation as both have been shown to be altered in LOAD. Methods: Human SKNMC neuronal cells and THP1 monocytes were infected in vitro for 24-72 hrs with a laboratory strain of Chlamydia …
Molecular Modeling And Sar Studies Of Cdk5/P25 Selective Inhibitors, Arindam Chatterjee
Molecular Modeling And Sar Studies Of Cdk5/P25 Selective Inhibitors, Arindam Chatterjee
Electronic Theses and Dissertations
Alzheimer's disease (AD) is one of the most dreaded forms of progressive neurodegenerative diseases. The two main hallmarks of AD are the formation of amyloid senile plaques and neurofibrillary tangles. Cyclin dependent kinase 5 (CDK5) is a proline directed serine/threonine kinase, which expressed primarily in the central nervous system. In the biochemical process the CDK5-natural activator, p35 is cleaved by calpain to a shorter protein p25, which in turn hyperphosphorylates Tau, forms neurofibrillary tangles and causes AD. CDK5 deregulation is also indicated in other neurodegenerative diseases, such as Huntington's chorea, stroke, Parkinson's disease, amyotrophic lateral sclerosis, major depression and substance …
Diet-Induced Ketosis And Calorie Restriction In Mouse Models Of Alzheimer's Pathology, Milene Lara Brownlow
Diet-Induced Ketosis And Calorie Restriction In Mouse Models Of Alzheimer's Pathology, Milene Lara Brownlow
USF Tampa Graduate Theses and Dissertations
Dietary manipulations and their pharmacological outcomes have been increasingly studied in neurodegenerative diseases. However, a systematic comparison among different methods in validated animal models of Alzheimer's disease is made necessary due to several different approaches applied in recent studies. Moreover, despite the large body of evidence on the effects of calorie restriction (CR) and ketogenic diets (KDs) on amyloid pathology, no consistent data is available on the effects of calorie restriction, ketogenic diet or ketone supplements on tau pathology in transgenic models of AD. Moreover, the ketogenic diet used in our studies was custom made with low carbohydrate content and …
Physical Mistreatment In Persons With Alzheimer’S Disease, Gregory Paveza, Carla Vandeweerd, Margaret Walsh, Jaime Corvin
Physical Mistreatment In Persons With Alzheimer’S Disease, Gregory Paveza, Carla Vandeweerd, Margaret Walsh, Jaime Corvin
Library Scholarship
Physical mistreatment has been estimated to affect 2 million older persons each year and dramatically affects health outcomes. While researchers have attempted to examine risk factors for specific forms of abuse, many have been able to focus on only victim or perpetrator characteristics, or a limited number of psychosocial variables at any one time. Additionally, data on risk factors for subgroups such as persons with Alzheimer’s disease who may have heightened and/or unique risk profiles has also been limited. This paper examines risk for physical violence in caregiver/patient dyads who participated in the Aggression and Violence in Community-Based Alzheimer’s Families …
The Role Of Histone Deacetylase Inhibitors In Ameliorating Memory Dysfunction Of An Alzheimer's Disease Mouse Model, Mark Kilgore
The Role Of Histone Deacetylase Inhibitors In Ameliorating Memory Dysfunction Of An Alzheimer's Disease Mouse Model, Mark Kilgore
All ETDs from UAB
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid beta plaques and neurofibrillary tangles, along with cognitive impairments that progress to dementia and eventually death. The development of drug treatments that rescue memory deficits could be a promising therapy given in the early stages of AD. In the following studies, we tested the potential for systemic treatment with histone deacetylase (HDAC) inhibitors to ameliorate cognitive deficits in a mouse model of AD. Using the APPSwe/PS1dE9 mouse model of AD, we showed that giving HDAC inhibitors systemically for 3 weeks reversed contextual memory deficits, stably maintained memories over a 2-week …