Affiliation: University of Michigan
- Mini-review: Retarding aging in murine genetic models of neurodegenerationRoger L Albin
Neurology Service and GRECC, VAAAHS, Ann Arbor, MI 48105, USA Dept of Neurology, University of Michigan, Ann Arbor, MI 48109, USA University of Michigan Udall Center for Parkinson s Disease Research, Ann Arbor, MI 48109, USA Michigan Alzheimer Disease Center, Ann Arbor, MI 48109, USA Electronic address
Neurobiol Dis 85:73-80. 2016..The experience with these models and interventions may be useful in designing future experiments assessing anti-aging interventions for disease-modifying treatment of neurodegenerative diseases. ..
- The role of serotonin in sleep disordered breathing associated with Parkinson disease: a correlative [11C]DASB PET imaging studyIrene M Lelieveld
Faculty of Psychology and Neuroscience, Maastricht University, Maastricht, The Netherlands
PLoS ONE 7:e40166. 2012..Neither serotoninergic nor dopaminergic neuron degeneration is likely to play a major role in SDB observed in PD patients...
- Assessing mild cognitive impairment with amyloid and dopamine terminal molecular imagingRoger L Albin
Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109 2200, USA
J Nucl Med 54:887-93. 2013..We evaluated PET-based classification of neurodegenerative pathology in mild cognitive impairment (MCI)...
- Initial agonist treatment of Parkinson disease: a critiqueRoger L Albin
Department of Neurology, Geriatric Research, Education, and Clinical Center, Ann Arbor VAMC, University of Michigan, Ann Arbor, USA
Neurology 60:390-4. 2003..The basic science supporting these rationales is equivocal. The clinical evidence for advantages of initial agonist treatment is incomplete. More data are required to determine the optimal initial treatment for PD...
- Diminished striatal [123I]iodobenzovesamicol binding in idiopathic cervical dystoniaRoger L Albin
Geriatrics Research, Education Clinical Center, Ann Arbor VAMC and Department of Neurology, University of Michigan 41809 0585, USA
Ann Neurol 53:528-32. 2003..Striatal [(131)I]iodobenzovesamicol binding was reduced. These results support a role for striatal dysfunction in idiopathic dystonias and suggest diminished striatal cholinergic interneuron density in cervical dystonia...
- Normal dopaminergic nigrostriatal innervation in SPG3A hereditary spastic paraplegiaRoger L Albin
Geriatrics Research, Education, and Clinical Center, Ann Arbor VAHS, Ann Arbor, Michigan 48109 2200, USA
J Neurogenet 22:289-94. 2008..This major difference between human SPG3A/atlastin-1 mutations and the Drosophila atl(l) phenotype has several possible explanations...
- Dominant ataxias and Friedreich ataxia: an updateRoger L Albin
Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
Curr Opin Neurol 16:507-14. 2003..This has resulted also in more rational classification schemes. Research on identified loci has begun to yield insights into the pathogenesis of neuronal dysfunction and neurodegeneration in these diseases...
- Increased ventral striatal monoaminergic innervation in Tourette syndromeR L Albin
Department of Neurology, The University of Michigan Medical School, Ann Arbor, USA
Neurology 61:310-5. 2003..Excessive striatal dopaminergic innervation is suggested to underlie Tourette syndrome (TS). Prior imaging and postmortem studies yield conflicting data...
- Spared caudal brainstem SERT binding in early Parkinson's diseaseRoger L Albin
Geriatrics Research, Education, and Clinical Center, Ann Arbor VA, Ann Arbor, MI, USA
J Cereb Blood Flow Metab 28:441-4. 2008..There was no asymmetry of diminished SERT binding. DASB binding in the medulla was relatively spared, inconsistent with the description of early prominent pathologic study in these caudal brainstem nuclei...
- Parkinson's disease: background, diagnosis, and initial managementRoger L Albin
Geriatrics Research, Education, and Clinical Center, Veterans Administration Medical Center, Ann Arbor, MI 48109 0585, USA
Clin Geriatr Med 22:735-51, v. 2006..Parkinson's disease is the most common disabling movement disorder. This article reviews the major clinical features, differential diagnosis, approach to diagnosis, and initial management of Parkinson's disease...
- Sham surgery controls are mitigated trolleysR L Albin
4412D Kresge III, 200 Zina Pitcher Place, Ann Arbor, MI 48109 0585, USA
J Med Ethics 31:149-52. 2005..I argue that sham surgery controls satisfy criteria derived from the trolley problem and are morally permissible...
- Striatal [11C]dihydrotetrabenazine and [11C]methylphenidate binding in Tourette syndromeR L Albin
Geriatrics Research, Education, and Clinical Center, Ann Arbor VAMC, Ann Arbor, MI, USA
Neurology 72:1390-6. 2009..Prior molecular imaging studies of nigrostriatal dopaminergic terminal markers report conflicting results. Our goal was to characterize the distribution of nigrostriatal dopaminergic terminals in subjects with TS...
- Comparing fludeoxyglucose F18-PET assessment of regional cerebral glucose metabolism and [11C]dihydrotetrabenazine-PET in evaluation of early dementia and mild cognitive impairmentRoger L Albin
VA Ann Arbor Health System Geriatrics Research, Education, and Clinical Center, and Department of Neurology, University of Michigan, Ann Arbor, MI 48109 2200, USA
Arch Neurol 67:440-6. 2010....
- Sham surgery controls: intracerebral grafting of fetal tissue for Parkinson's disease and proposed criteria for use of sham surgery controlsR L Albin
Department of Neurology, University of Michigan, 4412D Kresge III, 200 Zina Pitcher Place, Ann Arbor, MI 48109 0585, USA
J Med Ethics 28:322-5. 2002..Sham surgery controls, however, should be employed only when absolutely necessary. I suggest criteria for appropriate use of sham surgery controls...
- Decreased striatal dopaminergic innervation in REM sleep behavior disorderR L Albin
Department of Neurology, University of Michigan, Ann Arbor, USA
Neurology 55:1410-2. 2000..In subjects with RBD, there were significant reductions in striatal [11C]dihydrotetrabenazine binding, particularly in the posterior putamen...
- Rapid loss of striatal VMAT2 binding associated with onset of Lewy body dementiaRoger Albin
Department of Neurology, Geriatric Research, Ann Arbor, Michigan
Mov Disord 21:287-8. 2006
- Vesicular neurotransmitter transporters in Huntington's disease: initial observations and comparison with traditional synaptic markersM Suzuki
Department of Radiology (Division of Nuclear Medicine, The University of Michigan, Ann Arbor, Michigan, USA
Synapse 41:329-36. 2001..There is also markedly reduced expression of ChAT by surviving cholinergic striatal interneurons...
- Reliability of repeated cognitive assessment of dementia using a brief computerized batteryDustin Hammers
Neuropsychology Section, Department of Psychiatry, University of Michigan, Ann Arbor, USA
Am J Alzheimers Dis Other Demen 26:326-33. 2011..The aim of this study was to evaluate the short-term stability and reliability of a brief computerized cognitive battery in established dementia types...
- History of falls in Parkinson disease is associated with reduced cholinergic activityN I Bohnen
Department of Radiology, Division of Nuclear Medicine, University of Michigan, Ann Arbor 48105 9755, USA
Neurology 73:1670-6. 2009..To investigate the relationships between history of falls and cholinergic vs dopaminergic denervation in patients with Parkinson disease (PD)...
- Impact of belief in neuroprotection on therapeutic intervention in Parkinson's diseaseRodger J Elble
Department of Neurology, Southern Illinois University School of Medicine, Springfield, Illinois, USA
Mov Disord 25:1082-6. 2010..We found the investigators' level of confidence in these agents had no effect on the time to symptomatic therapy or on the change in UPDRS during 12 months of treatment...
- Astrocytic redox remodeling by amyloid beta peptideSanjay K Garg
Department of Biochemistry, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Antioxid Redox Signal 14:2385-97. 2011..Our study suggests that the alterations in astrocytic redox status could compromise the neuroprotective potential of astrocytes and may be a potential new target for therapeutic intervention in Alzheimer's disease...
- Myofibrillogenesis regulator 1 gene mutations cause paroxysmal dystonic choreoathetosisShirley Rainier
Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
Arch Neurol 61:1025-9. 2004..Previously, we and others identified a locus for autosomal dominant PDC on chromosome 2q33-2q35...
- Tetrahydro-9-aminoacridine (THA) interacts with the phencyclidine (PCP) receptor siteR L Albin
Department of Neurology, University of Michigan, Ann Arbor 48104
Neurosci Lett 88:303-7. 1988..THA may exert some of its clinical effects through interaction with the PCP receptor, and may have mixed agonist-antagonist properties...
- Receptor binding techniquesK A Frey
University of Michigan, Ann Arbor, Michigan, USA
Curr Protoc Neurosci . 2001..Quantification of the assay results can be accomplished by autoradiography or film densitometry. Finally, methods and considerations for analysis of the resulting data are presented...
- Chronic intrastriatal administration of quinolinic acid produces transient nocturnal hypermotility in the ratT J Bazzett
Department of Neurology, University of Michigan, Ann Arbor 48104 1687, USA
Brain Res Bull 39:69-73. 1996..With continued exposure, this behavioral effect may then diminish as a result of subsequent widespread striatal cell death...
- Alzheimer's disease versus dementia with Lewy bodies: cerebral metabolic distinction with autopsy confirmationS Minoshima
Department of Internal Medicine, University of Michigan Medical School, Geriatrics Research, Education, and Clinical Center, Ann Arbor, USA
Ann Neurol 50:358-65. 2001..In these patients, occipital hypometabolism preceded some clinical features of DLB. Occipital hypometabolism is a potential antemortem marker to distinguish DLB versus AD...
- Neuronal intranuclear inclusions and neuropil aggregates in HdhCAG(150) knockin miceS J Tallaksen-Greene
Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
Neuroscience 131:843-52. 2005..HdhCAG(150) knockin mice may be a model of early pathologic changes in HD...
- An advance in molecular imaging of dementiasRoger L Albin
Lancet Neurol 6:288-9. 2007
- Longitudinal evaluation of the Hdh(CAG)150 knock-in murine model of Huntington's diseaseMary Y Heng
Neuroscience Graduate Program and Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109, USA
J Neurosci 27:8989-98. 2007..The Hdh(CAG)150 knock-in mouse is a valid model to evaluate early events in the pathogenesis of neurodegeneration in HD...
- Hprt(CAG)146 mice: age of onset of behavioral abnormalities, time course of neuronal intranuclear inclusion accumulation, neurotransmitter marker alterations, mitochondrial function markers, and susceptibility to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridiSara J Tallaksen-Greene
Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109 0585, USA
J Comp Neurol 465:205-19. 2003..Hprt(CAG)146 mice did not exhibit increased susceptibility to the mitochondrial toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Hprt(CAG)146 mice are a useful model for studying polyglutamine repeat disorders...
- Mortalin: a protein associated with progression of Parkinson disease?Min Shi
Department of Pathology, University of Washington, School of Medicine, Seattle, Washington, USA
J Neuropathol Exp Neurol 67:117-24. 2008..Of those, mortalin, a mitochondrial protein, was decreased in the advanced PD cases and was further validated to be decreased using independent techniques. These results suggest a role for mortalin in PD progression...
- Brain imaging to assess the effects of dopamine agonists on progression of Parkinson diseaseRoger L Albin
JAMA 288:311-2; author reply 312-3. 2002
- Striatal monoaminergic terminals in Lewy body and Alzheimer's dementiasMasahiko Suzuki
Department of Radiology Nuclear Medicine, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109 0028, USA
Ann Neurol 51:767-71. 2002..We conclude that dementia with Lewy bodies may be distinguished from Alzheimer's disease by postmortem examination or by future in vivo measurements of the striatal vesicular monoamine transporter type 2...
- Cholinergic vesicular transporters in progressive supranuclear palsyMasahiko Suzuki
Department of Radiology, Division of Nuclear Medicine, University of Michigan, Ann Arbor, USA
Neurology 58:1013-8. 2002..To determine the status of cholinergic and monoaminergic vesicular transporter binding sites in progressive supranuclear palsy (PSP)...
- Treatment effects on nigrostriatal projection integrity in partial 6-OHDA lesions: comparison of L-DOPA and pramipexoleElyse S Kemmerer
Neuroscience Program, The University of Michigan, Ann Arbor, MI, USA
Exp Neurol 183:81-6. 2003..There was no treatment effect on VMAT2 expression in the partially lesioned striatum and thus no differential effect of indirect versus direct dopamimetic treatment on nigrostriatal integrity...
- Neuroimaging of Tourette syndromeKirk A Frey
Department of Neurology, The University of Michigan, Ann Arbor, MI 48109 0028, USA
J Child Neurol 21:672-7. 2006..Although the available data have important limitations, an encouraging convergence of findings implicates abnormal function in the Tourette syndrome striatum and in associated limbic and frontal cortical systems...
- Embryonic stem cells expressing expanded CAG repeats undergo aberrant neuronal differentiation and have persistent Oct-4 and REST/NRSF expressionMatthew T Lorincz
Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA
Mol Cell Neurosci 26:135-43. 2004..This novel model will allow analysis of the molecular pathogenesis of neuronal degeneration and can be used to rapidly screen therapeutic interventions for these fatal diseases...
- The mind's eye, looking inward? In search of executive control in internal attention shiftingWilliam J Gehring
Department of Psychology, University of Michigan, Ann Arbor, Michigan 48109 1109, USA
Psychophysiology 40:572-85. 2003..Bottom-up processes may include priming on no-switch trials and conflict on switch trials. Top-down processes may control conflict, subvocal rehearsal, and the contents of working memory...
- 11C-DTBZ and 18F-FDG PET measures in differentiating dementiasRobert A Koeppe
Division of Nuclear Medicine, Department of Radiology, University of Michigan School of Medicine, 3480 Kresge III, Box 0552, Ann Arbor, MI 48109, USA
J Nucl Med 46:936-44. 2005....
- Positron emission tomography of monoaminergic vesicular binding in aging and Parkinson diseaseNicolaas I Bohnen
Department of Radiology, Division of Nuclear Medicine, The University of Michigan Medical School, Ann Arbor, 48109 0028, USA
J Cereb Blood Flow Metab 26:1198-212. 2006..We conclude that (+)-[(11)C]DTBZ-PET imaging displays many properties necessary of a PD biomarker...
- Neuroimaging in dementia with Lewy bodies: metabolism, neurochemistry, and morphologySatoshi Minoshima
Departments of Radiology, University of Washington School of Medicine, Seattle, Washington 98195 6004, USA
J Geriatr Psychiatry Neurol 15:200-9. 2002....
- Genetics of subthalamic nucleus in development and diseaseSteven T Philips
Department of Pediatrics, The University of Michigan, Ann Arbor, MI 48109, USA
Exp Neurol 192:320-30. 2005..In this report, we discuss recent evidence for transcription factor mediated regulation of STN development. We also review STN developmental neurobiology and known patterns of gene expression in the developing and mature STN...
- Molecular and pathological effects of a modifier gene on deficiency of the sodium channel Scn8a (Na(v)1.6)Jennifer A Kearney
Department of Human Genetics, University of Michigan School of Medicine, Ann Arbor 48109, USA
Hum Mol Genet 11:2765-75. 2002..medJ mice provide a model for the physiological effects of sodium channel deficiency and the molecular mechanism of bigenic disease...
- Mutations in a novel gene encoding a CRAL-TRIO domain cause human Cayman ataxia and ataxia/dystonia in the jittery mouseJamee M Bomar
Mental Health Research Institute, 205 Zina Pitcher Place, University of Michigan, Ann Arbor, Michigan 48109 0720, USA
Nat Genet 35:264-9. 2003..Three-dimensional protein structural modeling predicts that the caytaxin ligand is more polar than vitamin E. Identification of the caytaxin ligand may help develop a therapy for Cayman ataxia...
- mGluRs: a target for pharmacotherapy in Parkinson diseaseJennifer A Feeley Kearney
Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
Exp Neurol 184:S30-6. 2003..Agents active at Group III mGluRs may also be useful for treatment of parkinsonism...
- A mutation in the human neurofilament M gene in Parkinson's disease that suggests a role for the cytoskeleton in neuronal degenerationChristian Lavedan
Novartis Pharmaceuticals Corporation, Pharmacogenetics, 9 W Watkins Mill Road, Gaithersburg, MD 20878, USA
Neurosci Lett 322:57-61. 2002..This finding suggests, for the first time, that aberrations in neuronal molecules involved in the cytoskeleton could lead to the development of the pathology seen in PD...
- Mice lacking phosphatidylinositol transfer protein-alpha exhibit spinocerebellar degeneration, intestinal and hepatic steatosis, and hypoglycemiaJames G Alb
Department of Cell and Developmental Biology, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599 7090, USA
J Biol Chem 278:33501-18. 2003..Taken together, the data suggest an unanticipated role for PITP alpha in with glucose homeostasis and in mammalian endoplasmic reticulum functions that interface with transport of specific luminal lipid cargoes...
- Optimal frequency for measuring health care resource utilization in Parkinson's disease using participant recall: the FS-TOO resource utilization substudyPatrick D Mauldin
Department of Clinical Pharmacy and Outcomes Sciences, Medical University of South Carolina, and the Ralph H Johnson VA Medical Center, Charleston, South Carolina 29425, USA
Clin Ther 30:1553-7. 2008....
- Dopamine and epilepsy: hints of complex subcortical rolesSheryl R Haut
Neurology 71:784-5. 2008
- Nucleocytoplasmic transport signals affect the age at onset of abnormalities in knock-in mice expressing polyglutamine within an ectopic protein contextWalker S Jackson
Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Hum Mol Genet 12:1621-9. 2003..Furthermore, the signals did not alter the relative regional distribution of NIIs, suggesting that factors other than nuclear access dictate the regional specificity of NII formation in this mouse model...
- Abnormalities of germ cell maturation and sertoli cell cytoskeleton in androgen receptor 113 CAG knock-in mice reveal toxic effects of the mutant proteinZhigang Yu
Department of Pathology, University of Michigan Medical School, 1301 Catherine, 4233 Medical Science 1, Ann Arbor, Michigan 48109, USA
Am J Pathol 168:195-204. 2006..Our data demonstrate that toxic effects of the mutant protein mediate aspects of the Kennedy disease phenotype previously attributed to a loss of AR function...
- Recent advances in Tourette syndrome researchRoger L Albin
Geriatrics Research, Education, and Clinical Center, Ann Arbor VAMC, Department of Neurology, University of Michigan, MI 48109, USA
Trends Neurosci 29:175-82. 2006..These lines of research have provided new pieces to the TS puzzle, and their increasing convergence is showing how those pieces can be put together...
- Proteomics identification of proteins in human cortex using multidimensional separations and MALDI tandem mass spectrometerSheng Pan
Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98104, USA
Mol Cell Proteomics 6:1818-23. 2007..Finally 140 proteins found in the cortical proteome were present in the proteome of cerebrospinal fluid, providing tissue-specific candidates for biomarker discovery in body fluid...
- Neurobiology of basal ganglia and Tourette syndrome: striatal and dopamine functionRoger L Albin
Department of Neurology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA
Adv Neurol 99:99-106. 2006
- Practice Parameters for Parkinson disease: signposts for clinical researchRoger L Albin
Neurology 66:966-7. 2006
- MURINE MODEL OF CAG REPEAT DISEASESRoger Albin; Fiscal Year: 2002..These experiments will establish HPRT-CAG mice as important tools for understanding neurodegeneration in CAG repeat diseases and enable accurate preclinical evaluation of interventions for CAG repeat diseases. ..
- Evaluating Striatal Function in a Murine HD ModelRoger Albin; Fiscal Year: 2007..Validation of these methods will provide new and useful behavioral tools for evaluating murine disease models. [unreadable] [unreadable] [unreadable]..