The Cellular Nucleic Acid Binding Protein Regulates The Alzheimer’S Disease Β-Secretase Protein Bace1,
2012
University of Kentucky
The Cellular Nucleic Acid Binding Protein Regulates The Alzheimer’S Disease Β-Secretase Protein Bace1, Christopher J. Holler
Theses and Dissertations--Molecular and Cellular Biochemistry
Alzheimer’s disease (AD) is the most common neurodegenerative disease affecting the elderly population and is believed to be caused by the overproduction and accumulation of the toxic amyloid beta (Aβ) peptide in the brain. Aβ is produced by two separate enzymatic cleavage events of the larger membrane bound amyloid precursor protein, APP. The first, and rate-limiting, cleavage event is made by beta-secretase, or BACE1, and is thus an attractive therapeutic target. Our lab, as well as many others, has shown that BACE1 protein and activity are increased in late-stage sporadic AD. We have extended these findings to show that BACE1 …
Bi-Lateral Changes To Hippocampal Cholesterol Levels During Epileptogenesis And In Chronic Epilepsy Following Focal-Onset Status Epilepticus In Mice,
2012
Technological University Dublin
Bi-Lateral Changes To Hippocampal Cholesterol Levels During Epileptogenesis And In Chronic Epilepsy Following Focal-Onset Status Epilepticus In Mice, Steve Meaney, Maura Heverin, Tobias Engel, Eva Jimenez-Mateosa, Reza Al-Aaudia, David Henshall
Articles
Brain cholesterol homeostasis has been shown to be disrupted in neurodegenerative conditions such as Alzheimer's and Huntington's diseases. Investigations in animal models of seizure-induced brain injury suggest that brain cholesterol levels are altered by prolonged seizures (status epilepticus) and are a feature of the pathophysiology of temporal lobe epilepsy. The present study measured hippocampal sterol levels in a model of unilateral hippocampal injury triggered by focal-onset status epilepticus, and in chronically epileptic mice. Status epilepticus was induced by intra-amygdala microinjection of kainic acid and ipsilateral and contralateral hippocampus analyzed. No significant changes were found for ipsilateral or contralateral hippocampal levels …
Triterpenoid Modulation Of Il-17 And Nrf-2 Expression Ameliorates Neuroinflammation And Promotes Remyelination In Autoimmune Encephalomyelitis,
2011
Case Western Reserve University
Triterpenoid Modulation Of Il-17 And Nrf-2 Expression Ameliorates Neuroinflammation And Promotes Remyelination In Autoimmune Encephalomyelitis, Tej K. Pareek, Abdelmadjid Belkadi, Sashi Kesavapany, Anita Zaremba, Sook L. Loh, Lianhua Bai, Mark L. Cohen, Colin Meyer, Karen T. Liby, Robert H. Miller, Michael B. Sporn, John J. Letterio
Dartmouth Scholarship
Inflammatory cytokines and endogenous anti-oxidants are variables affecting disease progression in multiple sclerosis (MS). Here we demonstrate the dual capacity of triterpenoids to simultaneously repress production of IL-17 and other pro-inflammatory mediators while exerting neuroprotective effects directly through Nrf2-dependent induction of anti-oxidant genes. Derivatives of the natural triterpene oleanolic acid, namely CDDO-trifluoroethyl-amide (CDDO-TFEA), completely suppressed disease in a murine model of MS, experimental autoimmune encephalomyelitis (EAE), by inhibiting Th1 and Th17 mRNA and cytokine production. Encephalitogenic T cells recovered from treated mice were hypo-responsive to myelin antigen and failed to adoptively transfer the disease. Microarray analyses showed significant suppression of …
Kate's Untested Baby (Huntington’S Disease And Abortion - Part Ii),
2011
University of San Diego
Kate's Untested Baby (Huntington’S Disease And Abortion - Part Ii), Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
An Angel Fighting For The Cure (Huntington’S Disease And Abortion - Part I),
2011
University of San Diego
An Angel Fighting For The Cure (Huntington’S Disease And Abortion - Part I), Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Role Of The Gcn5 Histone Acetyltransferase In Spinocerebellar Ataxia Type 7 And In Immature Neurons,
2011
The University of Texas Graduate School of Biomedical Sciences at Houston
Role Of The Gcn5 Histone Acetyltransferase In Spinocerebellar Ataxia Type 7 And In Immature Neurons, Yi Chun Chen
Dissertations and Theses (Open Access)
Spinocerebellar Ataxia type 7 (SCA7) is a neurodegenerative disease caused by expansion of a CAG repeat encoding a polyglutamine tract in ATXN7, a component of the SAGA histone acetyltransferase (HAT) complex. Previous studies provided conflicting evidence regarding the effects of polyQ-ATXN7 on the activity of Gcn5, the HAT catalytic subunit of SAGA. Here I showed that reducing Gcn5 expression accelerates both cerebellar and retinal degeneration in a mouse model of SCA7. Deletion of Gcn5 in Purkinje cells in mice expressing wild type Atxn7, however, causes only mild ataxia and does not lead to the early lethality observed in SCA7 mice. …
Multiple Sclerosis Is Not A Disease Of The Immune System,
2011
CUNY John Jay College
Multiple Sclerosis Is Not A Disease Of The Immune System, Angelique Corthals
Publications and Research
Multiple sclerosis is a complex neurodegenerative disease, thought to arise through autoimmunity against antigens of the central nervous system. The autoimmunity hypothesis fails to explain why genetic and environmental risk factors linked to the disease in one population tend to be unimportant in other populations. Despite great advances in documenting the cell and molecular mechanisms underlying MS pathophysiology, the autoimmunity framework has also been unable to develop a comprehensive explanation of the etiology of the disease. I propose a new framework for understanding MS as a dysfunction of the metabolism of lipids. Specifically, the homeostasis of lipid metabolism collapses during …
The Holy Grail Of Huntington's Disease Research: The Gene-Positive, Drug Trials, And Treatments,
2011
University of San Diego
The Holy Grail Of Huntington's Disease Research: The Gene-Positive, Drug Trials, And Treatments, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
An Hd Thanksgiving Toast,
2011
University of San Diego
An Hd Thanksgiving Toast, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Finding America’S Passion: The Nfl And Huntington’S Disease,
2011
University of San Diego
Finding America’S Passion: The Nfl And Huntington’S Disease, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Huntington’S Disease In The News And Entertainment Media - Part Ii: A Suicide On Tv,
2011
University of San Diego
Huntington’S Disease In The News And Entertainment Media - Part Ii: A Suicide On Tv, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Huntington’S Disease In The News And Entertainment Media - Part I: Stigma And Genetic Testing,
2011
University of San Diego
Huntington’S Disease In The News And Entertainment Media - Part I: Stigma And Genetic Testing, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Huntington’S Disease And The Financial Jitters,
2011
University of San Diego
Huntington’S Disease And The Financial Jitters, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Bdnf And ‘Neurobics’: Building A ‘Beautiful Mind’ Against Huntington's,
2011
University of San Diego
Bdnf And ‘Neurobics’: Building A ‘Beautiful Mind’ Against Huntington's, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Neuroprotective Effects Of Bilobalide Are Accompanied By A Reduction Of Ischemia-Induced Glutamate Release In Vivo,
2011
Goethe University Frankfurt
Neuroprotective Effects Of Bilobalide Are Accompanied By A Reduction Of Ischemia-Induced Glutamate Release In Vivo, Dorothee Lang, Cornelia Kiewert, Alexander Mdzinarishvili, Tina Maria Schwarzkopf, Rachita K. Sumbria, Joachim Hartmann, Jochen Klein
Pharmacy Faculty Articles and Research
Neuroprotective properties of bilobalide, a specific constituent of Ginkgo extracts, were tested in a mouse model of stroke. After 24 h of middle cerebral artery occlusion (MCAO), bilobalide reduced infarct areas in the core region (striatum) by 40–50% when given at 10 mg/kg 1 h prior to MCAO. Neuroprotection was also observed at lower doses, or when the drug was given 1 h past stroke induction. Sensorimotor function in mice was improved by bilobalide as shown by corner and chimney tests. When brain metabolism in situ was monitored by microdialysis, MCAO caused a rapid disappearance of extracellular glucose in the …
Making Sense Of Huntington’S Organizations, And A Call For Unity,
2011
University of San Diego
Making Sense Of Huntington’S Organizations, And A Call For Unity, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Waiting For Symptoms: How Long Can I Hang On?,
2011
University of San Diego
Waiting For Symptoms: How Long Can I Hang On?, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
One Man's Story: Entering The Light,
2011
University of San Diego
One Man's Story: Entering The Light, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Do-Or-Die Time For Huntington’S Clinical Trials,
2011
University of San Diego
Do-Or-Die Time For Huntington’S Clinical Trials, Kenneth P. Serbin
At Risk for Huntington's Disease
No abstract provided.
Upregulation Of Reactive Oxygen Species During The Retrovirus Life Cycle And Their Roles In A Mutant Of Moloney Murine Leukemia Virus, Ts1-Mediated Neurodegeneration,
2011
The University of Texas Graduate School of Biomedical Sciences at Houston
Upregulation Of Reactive Oxygen Species During The Retrovirus Life Cycle And Their Roles In A Mutant Of Moloney Murine Leukemia Virus, Ts1-Mediated Neurodegeneration, Soo Jin Kim
Dissertations and Theses (Open Access)
Viral invasion of the central nervous system (CNS) and development of neurological symptoms is a characteristic of many retroviruses. The mechanism by which retrovirus infection causes neurological dysfunction has yet to be fully elucidated. Given the complexity of the retrovirus-mediated neuropathogenesis, studies using small animal models are extremely valuable. Our laboratory has used a mutant moloney murine leukemia retrovirus, ts1-mediated neurodegneration. We hypothesize that astrocytes play an important role in ts1-induced neurodegeneration since they are retroviral reservoirs and supporting cells for neurons. It has been shown that ts1 is able to infect astrocytes in vivo and in …
