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Genomes and Genes | Mark A LovellSummaryAffiliation: University of Kentucky Country: USA Publications
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Publications
Induction of hyperphosphorylated tau in primary rat cortical neuron cultures mediated by oxidative stress and glycogen synthase kinase-3Mark A Lovell
Sanders Brown Center on Aging and Alzheimer s Disease Research Center, 101 Sanders Brown Bldg, University of Kentucky, Lexington, KY 40536 0230, USA
J Alzheimers Dis 6:659-71; discussion 673-81. 2004..Together these data suggest a culture model of hyperphosphorylated tau that implicates increased GSK-3 activity...- Amyloid beta peptide, 4-hydroxynonenal and apoptosisMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Curr Alzheimer Res 3:359-64. 2006..This review discusses current evidence supporting the role of oxidative stress/damage mediated apoptosis in in vitro models of neurodegeneration... - Oxidative damage in mild cognitive impairment and early Alzheimer's diseaseMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, Kentucky, USA
J Neurosci Res 85:3036-40. 2007..Because oxidative damage begins early in the progress of the disease, it represents a potential therapeutic target for slowing the onset and progression of AD... - Elevated zinc transporter-6 in mild cognitive impairment, Alzheimer disease, and pick diseaseMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, Kentucky, USA
J Neuropathol Exp Neurol 65:489-98. 2006..Increased ZnT-6 immunostaining in neurons containing cytoplasmic inclusions in MCI, AD, and PD suggests a role for ZnT-6 in the pathogenesis of these lesions... 
Oxidatively modified RNA in mild cognitive impairmentMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
Neurobiol Dis 29:169-75. 2008..In addition, levels of both adducts in MCI were comparable to those measured in LAD, suggesting RNA oxidation may be an early event in the pathogenesis of neuron degeneration in AD...- Ectopic expression of Musashi-1 in Alzheimer disease and Pick diseaseMark A Lovell
Department of Chemistry, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
J Neuropathol Exp Neurol 64:675-80. 2005..The presence of Msi-1 in a significant percentage of neurons containing cytoplasmic inclusions in 2 different neurodegenerative diseases suggests that it may play a role in the pathogenesis of these lesions... 
Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer's diseaseMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Nucleic Acids Res 35:7497-504. 2007....
An aberrant protein complex in CSF as a biomarker of Alzheimer diseaseM A Lovell
Department of Chemistry, Sanders Brown Center on Aging and Alzheimer s Disease Center, University of Kentucky, Lexington, KY 40536 0230, USA
Neurology 70:2212-8. 2008..To determine if an aberrant protein complex consisting of prostaglandin-d-synthase (PDS) and transthyretin (TTR) in CSF differentiates between subjects with Alzheimer disease (AD) and normal control (NC) subjects...- Quantitative proteomic analysis of mitochondria from primary neuron cultures treated with amyloid beta peptideMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Neurochem Res 30:113-22. 2005..Elevations of proteins associated with energy production suggest that cells undergoing Abeta-mediated apoptosis increase synthesis of proteins essential for ATP production and efflux in an attempt to maintain metabolic function... - Oxidatively modified nucleic acids in preclinical Alzheimer's disease (PCAD) brainMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Mech Ageing Dev 132:443-8. 2011..Overall, the data suggest oxidative damage to nucleic acids and a compensatory increase in OGG1 expression occur early in the pathogenesis of AD... - Organoselenium (Sel-Plex diet) decreases amyloid burden and RNA and DNA oxidative damage in APP/PS1 miceMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Free Radic Biol Med 46:1527-33. 2009..5). Overall, these data suggest that organic Se can reduce Abeta burden and minimize DNA and RNA oxidation and support a role for it as a potential therapeutic agent in neurologic disorders with increased oxidative stress... - Altered 8-oxoguanine glycosylase in mild cognitive impairment and late-stage Alzheimer's disease brainChangxing Shao
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
Free Radic Biol Med 45:813-9. 2008..Overall, our results suggest that decreased OGG1 activity occurs early in the progression of AD, possibly mediated by 4-hydroxynonenal inactivation and may contribute to elevated 8-OHdG in the brain in MCI and LAD... - Wilms' tumor suppressor (WT1) is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer's diseaseMark A Lovell
Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
Brain Res 983:84-96. 2003..Together, these data suggest a role for WT1 in the neurodegeneration observed in AD brain... - Seleno-L-methionine protects against beta-amyloid and iron/hydrogen peroxide-mediated neuron deathShuling Xiong
Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
Antioxid Redox Signal 9:457-67. 2007.... - Increased levels of 4-hydroxynonenal and acrolein, neurotoxic markers of lipid peroxidation, in the brain in Mild Cognitive Impairment and early Alzheimer's diseaseTaufika Islam Williams
Department of Chemistry, University of Kentucky, 135 Sanders-Brown Center on Aging, Lexington, KY 40506, USA
Neurobiol Aging 27:1094-9. 2006..We did not observe any statistically significant differences between MCI and EAD specimens. These results suggest that lipid peroxidation occurs early in the pathogenesis of AD... - Alterations of zinc transporter proteins ZnT-1, ZnT-4 and ZnT-6 in preclinical Alzheimer's disease brainGanna Lyubartseva
Department of Chemistry, Sanders Brown Center on Aging, Lexington, KY 40536, USA
Brain Pathol 20:343-50. 2010..Overall, our results suggest that alterations in Zn transport proteins may contribute to the pathology observed in PCAD subjects before onset of clinical symptoms... - Isolation of neural precursor cells from Alzheimer's disease and aged control postmortem brainMark A Lovell
Sanders Brown Center on Aging and Alzheimer s Disease Research Center, 800 S Limestone St, 101 Sanders Brown Bldg, University of Kentucky, Lexington, KY 40536 0230, USA
Neurobiol Aging 27:909-17. 2006..These results raise the possibility of stimulation of inherent precursor cells of aged individuals or AD patients to replace neurons lost in aging and/or neurodegeneration... - Elevated 4-hydroxyhexenal in Alzheimer's disease (AD) progressionMelissa A Bradley
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Neurobiol Aging 33:1034-44. 2012..Together these data support a role for lipid peroxidation in the progression of Alzheimer's disease... - Protection against amyloid beta peptide and iron/hydrogen peroxide toxicity by alpha lipoic acidMark A Lovell
Sanders Brown Center on Aging, University of Kentucky, 800 S Limestone St, Lexington, KY 40536 0230, USA
J Alzheimers Dis 5:229-39. 2003.... - Oxidative stress in head trauma in agingChangxing Shao
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Free Radic Biol Med 41:77-85. 2006..Glutathione reductase activity also showed an age-dependent decrease. Overall, our data show increased levels of oxidative damage, diminished antioxidant capacities, and increased tissue loss in TBI in aging... - Damage to lipids, proteins, DNA, and RNA in mild cognitive impairmentWilliam R Markesbery
Department of Neurology, University of Kentucky, Lexington, KY 40536 0230, USA
Arch Neurol 64:954-6. 2007..These studies establish oxidative damage as an early event in the pathogenesis of Alzheimer disease that can serve as a therapeutic target to slow the progression or perhaps the onset of the disease... - Detection and quantification of endogenous cyclic DNA adducts derived from trans-4-hydroxy-2-nonenal in human brain tissue by isotope dilution capillary liquid chromatography nanoelectrospray tandem mass spectrometryXinli Liu
Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506-0055, USA
Chem Res Toxicol 19:710-8. 2006..These results were consistent with the 32P postlabeling results, which detected 400-600 adducts per 10(9) normal nucleotides in the hippocampus... - Altered expression of zinc transporters-4 and -6 in mild cognitive impairment, early and late Alzheimer's disease brainJ L Smith
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Neuroscience 140:879-88. 2006..05) increased in hippocampus/parahippocampal gyrus of early Alzheimer's disease and Alzheimer's disease subjects. Zn transporter-6 is also increased (P<0.1) in the superior and middle temporal gyrus of Alzheimer's disease brain... - 4-Hydroxyhexenal (HHE) impairs glutamate transport in astrocyte culturesMark A Lovell
Department of Chemistry, University of Kentucky, Lexington, KY, USA
J Alzheimers Dis 32:139-46. 2012..Together these data suggest HHE can significantly impair glutamate uptake and may play a role in the pathogenesis of AD... - RNA oxidation adducts 8-OHG and 8-OHA change with Aβ42 levels in late-stage Alzheimer's diseaseAdam M Weidner
Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, United States of America
PLoS ONE 6:e24930. 2011..This study indicates that although there is a connection between AD related neuropathology and RNA oxidation, this relationship is not straightforward... - Increased oxidative damage in nuclear and mitochondrial DNA in mild cognitive impairmentJianquan Wang
Department of Chemistry, University of Kentucky, Lexington, KY 40536-0230, USA
J Neurochem 96:825-32. 2006..These results suggest that oxidative damage to nuclear and mitochondrial DNA occurs in the earliest detectable phase of AD and may play a meaningful role in the pathogenesis of this disease... - DNA oxidation in Alzheimer's diseaseWilliam R Markesbery
Department of Pathology and Laboratory Medicine, University of Kentucky, Lexington, Kentucky 40536 0230, USA
Antioxid Redox Signal 8:2039-45. 2006.... - Quantitative proteomic analysis of mitochondria in aging PS-1 transgenic miceYou Jun Fu
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
Cell Mol Neurobiol 29:649-64. 2009..The dysfunction of Na(+)/K(+) ATPase and signal transduction proteins may induce impaired cognition and memory before neurodegeneration occurs... - Quantitative changes in the mitochondrial proteome from subjects with mild cognitive impairment, early stage, and late stage Alzheimer's diseaseBert C Lynn
Department of Chemistry, University of Kentucky, Lexington, Kentucky, USA
J Alzheimers Dis 19:325-39. 2010..Comparison of protein changes throughout the progression of AD suggests the most pronounced changes occur in early AD mitochondria... - Procedure for the isolation of mitochondria, cytosolic and nuclear material from a single piece of neurological tissue for high-throughput mass spectral analysisMichael D Timmons
Department of Chemistry, University of Kentucky, Lexington, KY 40506 0046, USA
J Neurosci Methods 197:279-82. 2011.... - A potential role for alterations of zinc and zinc transport proteins in the progression of Alzheimer's diseaseMark A Lovell
Department of Chemistry and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
J Alzheimers Dis 16:471-83. 2009.... - 4-Hydroxynonenal oxidatively modifies histones: implications for Alzheimer's diseaseJennifer Drake
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
Neurosci Lett 356:155-8. 2004..Conceivably, altered DNA-histone interactions, subsequent to oxidative modification of histones by the lipid peroxidation product HNE, may contribute to the vulnerability of DNA to oxidation in AD brain... - Serum zinc in the progression of Alzheimer's diseaseJiang Dong
Department of Chemistry, University of Missouri, Columbia, MO, USA
J Alzheimers Dis 15:443-50. 2008..Overall, these data suggest a significant decrease of serum Zn in men with MCI, may explain the loss of ZnT-1 observed in previous studies and suggest there may be more pronounced sex differences in MCI than were previously recognized... - Analysis of derivatized biogenic aldehydes by LC tandem mass spectrometryTaufika Islam Williams
Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506, USA
Anal Chem 77:3383-9. 2005..The LC-MS/MS methodology developed here will be used in subsequent studies to determine aldehyde concentrations for comparing age-matched controls to AD tissues from human subjects... - Lipid peroxidation is an early event in the brain in amnestic mild cognitive impairmentWilliam R Markesbery
Alzheimer s Disease Research Center, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
Ann Neurol 58:730-5. 2005..Our data indicate that lipid peroxidation is present in the brain of MCI patients and suggest that oxidative damage may play a role in the pathogenesis of AD... - Development of a method for quantification of acrolein-deoxyguanosine adducts in DNA using isotope dilution-capillary LC/MS/MS and its application to human brain tissueXinli Liu
Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506-0055, USA
Anal Chem 77:5982-9. 2005..Statistically significant differences (P < 0.05) in levels of Acro-dG between AD subjects and controls were observed in DNA isolated from the hippocampus/parahippocampal gyrus... - White matter diffusion alterations in normal women at risk of Alzheimer's diseaseCharles D Smith
Department of Neurology, University of Kentucky, Lexington, KY 40536, USA
Neurobiol Aging 31:1122-31. 2010..These findings demonstrate that specific white matter pathways are altered in normal women at increased risk of AD years before the expected onset of cognitive symptoms... - Ratio of 8-hydroxyguanine in intact DNA to free 8-hydroxyguanine is increased in Alzheimer disease ventricular cerebrospinal fluidM A Lovell
University of Kentucky, Department of Chemistry, Sanders Brown Center on Aging, 101 Sanders Brown Bldg, 800 S Limestone St, Lexington, KY 40536 0230, USA
Arch Neurol 58:392-6. 2001.... - Protection against amyloid beta peptide toxicity by zincM A Lovell
Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
Brain Res 823:88-95. 1999..Together, these data suggest that Zn functions as a double-edged sword, affording protection against Abeta at low concentrations and enhancing toxicity at high concentrations... - Glomerular lesions in male rabbits treated with aluminium lactate: with special reference to microaneurysm formationC B Hong
Department of Veterinary Science, University of Kentucky, Lexington 40511, USA
Exp Toxicol Pathol 52:139-43. 2000..The sclerotic change is interpreted as a sequela of microaneurysm. The findings suggest that aluminum induces glomerular lesions in rabbits. This may serve as a good animal model to study mesangiolysis and microaneurysm formation... - Alterations in zinc transporter protein-1 (ZnT-1) in the brain of subjects with mild cognitive impairment, early, and late-stage Alzheimer's diseaseM A Lovell
Sanders Brown Center on Aging and Departments of Chemistry, Neurology and Pathology, University of Kentucky, Lexington, KY 40536, USA
Neurotox Res 7:265-71. 2005.... - Increased oxidative damage in nuclear and mitochondrial DNA in Alzheimer's diseaseJ Wang
Department of Chemistry, University of Kentucky, Lexington, 40536, USA
J Neurochem 93:953-62. 2005..DNA from temporal lobe showed the most oxidative damage, whereas cerebellum was only slightly affected in AD brains. These results suggest that oxidative damage to mitochondrial DNA may contribute to the neurodegeneration of AD... - Decreased base excision repair and increased helicase activity in Alzheimer's disease brainM A Lovell
Sanders Brown Center on Aging and Alzheimer s Disease Research Center, 101 Sanders Brown Building, University of Kentucky, 800 South Limestone Street, Lexington, KY 40536 0230, USA
Brain Res 855:116-23. 2000..The modest increase in DNA helicase activity in some brain regions in AD may interfere with base excision repair mechanisms. Overall, the decreased repair of DNA damage could be involved in the pathogenesis of neurodegeneration in AD... - Longitudinal functional alterations in asymptomatic women at risk for Alzheimer's diseaseC D Smith
Department of Neurology, Magnetic Resonance Imaging Spectrometry Center Davis Mills Room 62, University of Kentucky Medical Center, 800 Rose Street, Lexington, KY 40536, USA
J Neuroimaging 15:271-7. 2005..The authors sought to determine whether known alterations of brain function in normal individuals who are at high risk for Alzheimer's disease (AD) worsen or stay the same after a significant interval of time... - Decreased thioredoxin and increased thioredoxin reductase levels in Alzheimer's disease brainM A Lovell
Sanders Brown Center on Aging, Departments of Chemistry, Neurology, and Pathology, University of Kentucky, Lexington, KY 40536 0230, USA
Free Radic Biol Med 28:418-27. 2000..This decrease in the antioxidant Trx-TR system may contribute to the increased oxidative stress and subsequent neurodegeneration observed in the brain in AD... - Use of bomb pulse carbon-14 to age senile plaques and neurofibrillary tangles in Alzheimer's diseaseMark A Lovell
From the Sanders Brown Center on Aging and Alzheimer s Disease Research Center, 101 Sanders Brown Bldg, University of Kentucky, Lexington 40536 0230, USA
Neurobiol Aging 23:179-86. 2002..In addition, the data show that these structures, once formed, have a much slower carbon turnover rate than normal brain and are not in a formation/enzymatic degradation equilibrium... - 4-Hydroxynonenal disrupts zinc export in primary rat cortical cellsJ L Smith
Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
Neurotoxicology 27:1-5. 2006..05) increase of (65)Zn was observed inside cortical neurons after treatment with 20 microM HNE for 4 hours. These data suggest that HNE may impair a protein essential for zinc export leading to increased levels of intracellular zinc... - Proteomic analysis of human ventricular cerebrospinal fluid from neurologically normal, elderly subjects using two-dimensional LC-MS/MSBrett R Wenner
Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506-0055, USA
J Proteome Res 3:97-103. 2004..Of these proteins, 38% were unique to individual subjects, whereas only 6% were common to all 10 subjects. These results suggest considerable subject-to-subject variability in the CSF proteome... - APOE is a potential modifier gene in an autosomal dominant form of frontotemporal dementia (IBMPFD)Sarju G Mehta
Children s Hospital Clinical Genetics and Metabolism, Boston, Massachusetts, and Department of Neurology and Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
Genet Med 9:9-13. 2007..Modifier genes could account for decreased frontotemporal dementia penetrance. In this study apolipoprotein-E (APOE) was evaluated for this role in IBMPFD families based on its known modifier effect in Alzheimer's disease... - Identification and characterization of OGG1 mutations in patients with Alzheimer's diseaseGuogen Mao
Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA
Nucleic Acids Res 35:2759-66. 2007..Our findings suggest that defects in OGG1 may be important in the pathogenesis of AD in a significant fraction of AD patients and provide new insight into the molecular basis for the disease... - Acrolein is increased in Alzheimer's disease brain and is toxic to primary hippocampal culturesM A Lovell
Sanders-Brown Center on Aging and Alzheimer's Disease Research Center, 101 Sanders-Brown Building, University of Kentucky, 800 South Limestone Street, Lexington, KY 40536-0230, USA
Neurobiol Aging 22:187-94. 2001..Collectively, these data show that acrolein is increased in the brain in AD and demonstrate neurotoxicity mechanisms that might be important in the pathogenesis of neuron degeneration in AD... - Expression of glutathione-S-transferase isozyme in the SY5Y neuroblastoma cell line increases resistance to oxidative stressC Xie
Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536-0230, USA
Free Radic Biol Med 31:73-81. 2001..These results suggest that overexpression of GST increases resistance to endogenous HNE induced by oxidative stress or released in the degradation of 1,1,4-tris (acetyloxy)nonane, but not to exogenous application of HNE... - University of Kentucky Sanders-Brown healthy brain aging volunteers: donor characteristics, procedures and neuropathologyFrederick A Schmitt
Department of Neurology and the Sanders Brown Center on Aging, 303 Sanders Brown Building, 800 S Limestone, University of Kentucky, Lexington, USA
Curr Alzheimer Res 9:724-33. 2012..We also explain some of the evolving methodologies and the academic contributions that have been made due to this motivated group of older Kentuckians... - Increased levels of 4-hydroxynonenal and acrolein in the brain in preclinical Alzheimer diseaseM A Bradley
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
Free Radic Biol Med 48:1570-6. 2010..Additionally, no significant differences in levels of protein carbonyls were observed in the HPG, SMTG, or CER of PCAD subjects compared to NC subjects... - Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse modelsJoshua A Sonnen
Department of Pathology and of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA, USA
Free Radic Biol Med 45:219-30. 2008..Future efforts in preclinical models and ultimately clinical trials are needed to define optimally effective agents and combinations, doses, and timing to suppress safely this facet of AD...