Eileen H Bigio

Summary

Affiliation: Northwestern University
Country: USA

Publications

  1. pmc TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson's disease
    Sruti Rayaprolu
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
    Mol Neurodegener 8:19. 2013
  2. pmc Frontotemporal lobar degeneration with TDP-43 proteinopathy and chromosome 9p repeat expansion in C9ORF72: clinicopathologic correlation
    Eileen H Bigio
    Cognitive Neurology and Alzheimer Disease Center, Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA
    Neuropathology 33:122-33. 2013
  3. pmc Making the diagnosis of frontotemporal lobar degeneration
    Eileen H Bigio
    Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
    Arch Pathol Lab Med 137:314-25. 2013
  4. pmc TDP-43 pathology in primary progressive aphasia and frontotemporal dementia with pathologic Alzheimer disease
    Eileen H Bigio
    Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
    Acta Neuropathol 120:43-54. 2010
  5. pmc Update on recent molecular and genetic advances in frontotemporal lobar degeneration
    Eileen H Bigio
    Department of Pathology, Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, 710 N Fairbanks Court, Chicago, IL 60611, USA
    J Neuropathol Exp Neurol 67:635-48. 2008
  6. ncbi request reprint Synapse loss may be a minor contributor to decreased regional cerebral blood flow in Alzheimer disease
    Eileen H Bigio
    Department of Pathology, Northwestern University Medical School, Chicago, Ill 60611, USA
    Dement Geriatr Cogn Disord 15:72-8. 2003
  7. pmc TDP-43 variants of frontotemporal lobar degeneration
    Eileen H Bigio
    Department of Pathology and Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
    J Mol Neurosci 45:390-401. 2011
  8. ncbi request reprint Synapse loss is greater in presenile than senile onset Alzheimer disease: implications for the cognitive reserve hypothesis
    Eileen H Bigio
    Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611, USA
    Neuropathol Appl Neurobiol 28:218-27. 2002
  9. pmc Differential involvement of optineurin in amyotrophic lateral sclerosis with or without SOD1 mutations
    Han Xiang Deng
    Division of Neuromuscular Medicine, Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
    Arch Neurol 68:1057-61. 2011
  10. pmc Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia
    Han Xiang Deng
    Division of Neuromuscular Medicine, Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA
    Nature 477:211-5. 2011

Detail Information

Publications52

  1. pmc TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson's disease
    Sruti Rayaprolu
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
    Mol Neurodegener 8:19. 2013
    ..With this in mind we set out to assess the genetic association of the Alzheimer's disease-related risk variant in TREM2 (rs75932628, p.R47H) with other related neurodegenerative disorders...
  2. pmc Frontotemporal lobar degeneration with TDP-43 proteinopathy and chromosome 9p repeat expansion in C9ORF72: clinicopathologic correlation
    Eileen H Bigio
    Cognitive Neurology and Alzheimer Disease Center, Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA
    Neuropathology 33:122-33. 2013
    ....
  3. pmc Making the diagnosis of frontotemporal lobar degeneration
    Eileen H Bigio
    Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
    Arch Pathol Lab Med 137:314-25. 2013
    ..The 2 major categories of pathologic FTLD are tauopathies (FTLD-tau) and ubiquitinopathies (FTLD-U). Pick disease is one of the FTLD-tau subtypes and is termed FTLD-tau (PiD)...
  4. pmc TDP-43 pathology in primary progressive aphasia and frontotemporal dementia with pathologic Alzheimer disease
    Eileen H Bigio
    Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
    Acta Neuropathol 120:43-54. 2010
    ..Furthermore, medial temporal TDP-43 pathology is more tightly linked to HS than to clinical phenotype. These findings challenge the current notions about clinicopathologic correlation, especially about the role of multiple pathologies...
  5. pmc Update on recent molecular and genetic advances in frontotemporal lobar degeneration
    Eileen H Bigio
    Department of Pathology, Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, 710 N Fairbanks Court, Chicago, IL 60611, USA
    J Neuropathol Exp Neurol 67:635-48. 2008
    ..This review highlights the neuropathologic features and the most important discoveries of the last 2 years and places these findings into the historical context of FTLD...
  6. ncbi request reprint Synapse loss may be a minor contributor to decreased regional cerebral blood flow in Alzheimer disease
    Eileen H Bigio
    Department of Pathology, Northwestern University Medical School, Chicago, Ill 60611, USA
    Dement Geriatr Cogn Disord 15:72-8. 2003
    ..The results of this study suggest that synapse loss may be a minor contributor to the decreased rCBF observed in AD...
  7. pmc TDP-43 variants of frontotemporal lobar degeneration
    Eileen H Bigio
    Department of Pathology and Cognitive Neurology and Alzheimer Disease Center, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
    J Mol Neurosci 45:390-401. 2011
    ..In this paper, FTLD-TDP pathologic sub-types will be described, and examples of each sub-type will be shown, and implications for future research will be discussed...
  8. ncbi request reprint Synapse loss is greater in presenile than senile onset Alzheimer disease: implications for the cognitive reserve hypothesis
    Eileen H Bigio
    Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611, USA
    Neuropathol Appl Neurobiol 28:218-27. 2002
    ..The differences in synapse loss and Alzheimer-type pathology in presenile and senile onset AD support the hypothesis that 'cognitive reserve' protects the human brain from neurodegenerative disease...
  9. pmc Differential involvement of optineurin in amyotrophic lateral sclerosis with or without SOD1 mutations
    Han Xiang Deng
    Division of Neuromuscular Medicine, Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
    Arch Neurol 68:1057-61. 2011
    ..Mutations in optineurin have recently been linked to amyotrophic lateral sclerosis (ALS)...
  10. pmc Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia
    Han Xiang Deng
    Division of Neuromuscular Medicine, Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA
    Nature 477:211-5. 2011
    ....
  11. pmc Alzheimer and frontotemporal pathology in subsets of primary progressive aphasia
    Marsel Mesulam
    Cognitive Neurology and Alzheimer s Disease Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
    Ann Neurol 63:709-19. 2008
    ..To identify predictors of Alzheimer's disease (AD) versus frontotemporal lobar degeneration pathology in primary progressive aphasia (PPA), and determine whether the AD pathology is atypically distributed to fit the aphasic phenotype...
  12. ncbi request reprint Gene expression analysis of frontotemporal lobar degeneration of the motor neuron disease type with ubiquitinated inclusions
    Manjari Mishra
    Cognitive Neurology and Alzheimer Disease Center, Northwestern University, Feinberg School of Medicine, 320 East Superior St, Chicago, IL, 60611, USA
    Acta Neuropathol 114:81-94. 2007
    ..Our findings point to specific gene-linked-pathways which may be influenced by neurodegenerative disease process and may be targeted for further exploration...
  13. ncbi request reprint Tau nitration occurs at tyrosine 29 in the fibrillar lesions of Alzheimer's disease and other tauopathies
    Matthew R Reynolds
    Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
    J Neurosci 26:10636-45. 2006
    ..Collectively, our findings provide the first direct evidence that site-specific tau nitration is linked to the progression of the neurodegenerative tauopathies...
  14. doi request reprint FUS-immunoreactive inclusions are a common feature in sporadic and non-SOD1 familial amyotrophic lateral sclerosis
    Han Xiang Deng
    Division of Neuromuscular Medicine, Davee Department of Neurology and Clinical Neurosciences, Chicago, IL 60611, USA
    Ann Neurol 67:739-48. 2010
    ..The pathogenic mechanism of the mutant FUS-mediated ALS and potential roles of FUS in non-FUS ALS remain to be investigated...
  15. pmc TAR DNA-binding protein 43 immunohistochemistry reveals extensive neuritic pathology in FTLD-U: a midwest-southwest consortium for FTLD study
    Kimmo J Hatanpaa
    Department of Pathology, University of Texas Southwestern School of Medicine, Dallas, Texas 75390, USA
    J Neuropathol Exp Neurol 67:271-9. 2008
    ..Moreover, assessment of abnormalities in both the hippocampus and frontal cortex may be diagnostically important in FTLD-U...
  16. pmc Calpain-mediated tau cleavage: a mechanism leading to neurodegeneration shared by multiple tauopathies
    Adriana Ferreira
    Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
    Mol Med 17:676-85. 2011
    ..Collectively, these data suggest that the mechanism underlying the generation of the 17-kDa neurotoxic tau fragment might be part of a conserved pathologic process shared by multiple tauopathies...
  17. pmc National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease: a practical approach
    Thomas J Montine
    Department of Pathology, University of Washington School of Medicine, Box 359791, Seattle, WA 98104, USA
    Acta Neuropathol 123:1-11. 2012
    ..Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations...
  18. doi request reprint Detection of protein aggregation in neurodegenerative diseases
    Han Xiang Deng
    Division of Neuromuscular Medicine, Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
    Methods Mol Biol 793:259-72. 2011
    ..Using this method, we successfully detected some protein aggregates that escaped detection when other antigen-retrieval methods were employed...
  19. ncbi request reprint West Nile virus encephalomyelitis with polio-like paralysis & nigral degeneration
    Kristian T Schafernak
    Division of Neuropathology, Northwestern University Feinberg School of Medicine, 710 N Fairbanks Court, Olson 3 459, Chicago, Illinois 60611, USA
    Can J Neurol Sci 33:407-10. 2006
    ..Movement disorders have also been described...
  20. ncbi request reprint Progranulin mutations in primary progressive aphasia: the PPA1 and PPA3 families
    Marsel Mesulam
    Cognitive Neurology and Alzheimer s Disease Center and Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ill 60611, USA
    Arch Neurol 64:43-7. 2007
    ..Primary progressive aphasia (PPA) is a language-based dementia characterized by fluent or nonfluent language disorder as its principal feature...
  21. doi request reprint Asymmetry and heterogeneity of Alzheimer's and frontotemporal pathology in primary progressive aphasia
    M Marsel Mesulam
    Cognitive Neurology and Alzheimer s Disease Centre, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA
    Brain 137:1176-92. 2014
    ..Revisions of criteria for logopenic primary progressive aphasia are proposed to address these challenges. ..
  22. pmc Conversion to the amyotrophic lateral sclerosis phenotype is associated with intermolecular linked insoluble aggregates of SOD1 in mitochondria
    Han Xiang Deng
    Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Tarry Building, Room 13 715, 303 East Chicago Avenue, Chicago, IL 60611, USA
    Proc Natl Acad Sci U S A 103:7142-7. 2006
    ..Importantly, rational therapy based on these observations can now be developed and tested...
  23. pmc Correlation of Alzheimer disease neuropathologic changes with cognitive status: a review of the literature
    Peter T Nelson
    Sanders Brown Center on Aging, Department of Pathology, University of Kentucky, Lexington 40536 0230, USA
    J Neuropathol Exp Neurol 71:362-81. 2012
    ..Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles...
  24. doi request reprint Alterations of Ca(2+)-responsive proteins within cholinergic neurons in aging and Alzheimer's disease
    David Riascos
    Cognitive Neurology and Alzheimer s Disease Center, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
    Neurobiol Aging 35:1325-33. 2014
    ..Substantial age- and AD-related alterations in Ca(2+)-sensing proteins most likely contribute to selective vulnerability of BFCN to degeneration in AD. ..
  25. doi request reprint Pineal chordoid meningioma complicated by repetitive hemorrhage during pregnancy: case report and literature review
    Kyung Hwa Lee
    Department of Pathology, Northwestern University McGaw Medical Center, Chicago, Illinois 60611, USA
    Neuropathology 33:192-8. 2013
    ..Additionally, there was abundant lymphoplasmacytic infiltration within the tumor. The details of this case are presented with a review of the literature...
  26. ncbi request reprint Tau truncation during neurofibrillary tangle evolution in Alzheimer's disease
    Angela L Guillozet-Bongaarts
    Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, 303 E Chicago Avenue, Chicago, IL 60611, USA
    Neurobiol Aging 26:1015-22. 2005
    ....
  27. pmc Nuclear Carrier and RNA Binding Proteins in Frontotemporal Lobar Degeneration associated with Fused in Sarcoma (FUS) pathological changes
    Yvonne S Davidson
    Mental Health and Neurodegeneration Research Group, Faculty of Human and Medical Sciences, University of Manchester, Manchester, UK Northwestern CNADC Neuropathology Core, Northwestern University Feinberg School of Medicine, Chicago, USA Department of Neuropathology, Walton Centre for Neurology and Neurosurgery, Liverpool, UK Neuropathology Cellular Pathology, Royal Victoria Infirmary, Newcastle upon Tyne, UK Institute for Ageing and Health, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, UK Departments of Neurology and Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA Cerebral Function Unit, Greater Manchester Neuroscience Centre, Salford Royal Foundation Trust, UK
    Neuropathol Appl Neurobiol . 2012
    ..2012 The Authors. Neuropathology and Applied Neurobiology © 2012 British Neuropathological Society...
  28. ncbi request reprint Neuronal ubiquitinated intranuclear inclusions in familial and non-familial frontotemporal dementia of the motor neuron disease type associated with amyotrophic lateral sclerosis
    Eileen H Bigio
    Northwestern Cognitive Neurology and Alzheimer Disease Center, and Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA
    J Neuropathol Exp Neurol 63:801-11. 2004
    ..In addition, the current study confirms that Ub-INIs are found in familial FTD-MND-type, but also extends the presence of Ub-INIs to familial FTD-MND (with concomitant ALS), and probably also to non-familial FTD-MND-type...
  29. pmc Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis
    Nicola J Rutherford
    Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, United States of America
    PLoS Genet 4:e1000193. 2008
    ....
  30. pmc TAR DNA-binding protein-43 in amyotrophic lateral sclerosis, frontotemporal lobar degeneration, and Alzheimer disease
    Eileen H Bigio
    Acta Neuropathol 116:135-40. 2008
  31. ncbi request reprint Lateralization on neuroimaging does not differentiate frontotemporal lobar degeneration from Alzheimer's disease
    Anne M Lipton
    Alzheimer s Disease Centers at The University of Texas Southwestern Medical Center, Dallas, Tex, USA
    Dement Geriatr Cogn Disord 17:324-7. 2004
    ..Three of 4 FTLD cases had lateralized atrophy on CT. For the AD cases, 10/17 SPECTs, 2/7 MRIs, and 1/9 CTs showed lateralized findings. Of the neuroimaging modalities utilized, SPECT was the most sensitive in detecting lateralization...
  32. pmc Association of GSK3B with Alzheimer disease and frontotemporal dementia
    Barbara A J Schaffer
    Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, 2506 Gonda, 695 Charles E Young Dr S, Los Angeles, CA 90095 1761, USA
    Arch Neurol 65:1368-74. 2008
    ..As a known tau kinase, GSK3B is a promising candidate gene in the remaining cases of FTD and in AD, for which tau mutations have not been found...
  33. pmc TDP-43 A315T mutation in familial motor neuron disease
    Michael A Gitcho
    Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 63:535-8. 2008
    ..The discovery of a missense mutation in TDP-43 in a family with dominantly inherited motor neuron disease provides evidence of a direct link between altered TDP-43 function and neurodegeneration...
  34. ncbi request reprint The L266V tau mutation is associated with frontotemporal dementia and Pick-like 3R and 4R tauopathy
    Marion Hogg
    Neurogenetics Laboratory, Mayo Clinic Jacksonville, Jacksonville, Florida, USA
    Acta Neuropathol 106:323-36. 2003
    ..In addition, the results of the RD3 and ET3 immunostains clearly explain for the first time the presence of both 3R and 4R tau isoforms in preparations of insoluble tau from some Pick's disease cases...
  35. ncbi request reprint Frontotemporal lobar degeneration with motor neuron disease-type inclusions predominates in 76 cases of frontotemporal degeneration
    Anne M Lipton
    Department of Neurology, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd, Dallas, TX 75390 9129, USA
    Acta Neuropathol 108:379-85. 2004
    ..Only eight (11%) were classified as Pick's disease. Several cases originally designated as DLDH could be reclassified as FTLD-MND-type based on current recommendations for classification of FTD...
  36. ncbi request reprint Synaptic targeting by Alzheimer's-related amyloid beta oligomers
    Pascale N Lacor
    Neurobiology and Physiology Department, Northwestern University, Evanston, Illinois 60208, USA5
    J Neurosci 24:10191-200. 2004
    ..Results suggest the hypothesis that targeting and functional disruption of particular synapses by Abeta oligomers may provide a molecular basis for the specific loss of memory function in early AD...
  37. ncbi request reprint Mutation analysis of patients with neuronal intermediate filament inclusion disease (NIFID)
    Parastoo Momeni
    Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, Building 35 Room 1A1010 35 Convent Drive, Bethesda, MD 20892, USA
    Neurobiol Aging 27:778.e1-778.e6. 2006
    ..To determine the molecular genetic contribution to this disease we performed a mutation analysis of all type IV neuronal IF, SOD1 and NUDEL genes in cases of NIFID and unaffected control cases. We found no pathogenic variants...
  38. ncbi request reprint Letter to the editor
    Nigel J Cairns
    J Neuropathol Exp Neurol 65:97; author reply 97-8. 2006
  39. ncbi request reprint An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies
    Rohan de Silva
    Reta Lila Weston Institute of Neurological Studies, University College London, Windeyer Building, 46 Cleveland St, W1T 4JF, London, UK
    Acta Neuropathol 111:329-40. 2006
    ..The use of such tau isoform specific antibodies may refine pathological criteria underpinning FTLD...
  40. ncbi request reprint Tc-99m HMPAO SPECT in the differential diagnosis of the dementias with histopathologic confirmation
    Frederick J Bonte
    Nuclear Medicine Center, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390 9061, USA
    Clin Nucl Med 31:376-8. 2006
    ..The purpose of this study is to determine the value of Tc-99m HMPAO SPECT in the diagnosis of the dementias, with particular reference to Alzheimer disease...
  41. ncbi request reprint Monoclonal antibodies that target pathological assemblies of Abeta
    Mary P Lambert
    Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA
    J Neurochem 100:23-35. 2007
    ....
  42. ncbi request reprint Cognitive impairment, frontotemporal dementia, and the motor neuron diseases
    Michael J Strong
    Department of Clinical Neurological Sciences and the Robarts Research Institute, London, Ontario, Canada
    Ann Neurol 54:S20-3. 2003
  43. pmc Molecular characterization of novel progranulin (GRN) mutations in frontotemporal dementia
    Odity Mukherjee
    Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Hum Mutat 29:512-21. 2008
    ....
  44. ncbi request reprint Phenotypic variability associated with progranulin haploinsufficiency in patients with the common 1477C-->T (Arg493X) mutation: an international initiative
    Rosa Rademakers
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Lancet Neurol 6:857-68. 2007
    ..The most common mutation in GRN is Arg493X. We aimed to establish the contribution of this mutation to FTLD and related disorders...
  45. pmc TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions
    Nigel J Cairns
    MRCPath, Department of Pathology and Immunology, Washington University School of Medicine, Campus Box 8118, St Louis, MO 63110, USA
    Am J Pathol 171:227-40. 2007
    ....
  46. pmc Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration
    Nigel J Cairns
    Department of Neurology, Washington University School of Medicine, Campus Box 8118, 660 South Euclid Avenue, St Louis, MO, 63110, USA
    Acta Neuropathol 114:5-22. 2007
    ..These criteria will be of value to the practicing neuropathologist and provide a foundation for clinical, clinico-pathologic, mechanistic studies and in vivo models of pathogenesis of FTLD...
  47. ncbi request reprint Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations
    Ian R A Mackenzie
    Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
    Ann Neurol 61:427-34. 2007
    ..We recently identified TDP-43 as the major pathological protein in sporadic ALS. In this study, we investigated TDP-43 in a larger series of ALS cases (n = 111), including familial cases with and without SOD1 mutations...
  48. pmc Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers
    Fernanda G De Felice
    Department of Neurobiology and Physiology, Northwestern University, 2205 Tech Drive, Evanston, IL 60208, USA
    Neurobiol Aging 29:1334-47. 2008
    ..A beta oligomers have been increasingly implicated as the main neurotoxins in AD, and the current results provide a unifying mechanism in which oligomer activity is directly linked to tau hyperphosphorylation in AD pathology...
  49. pmc Neuronal intranuclear inclusions are ultrastructurally and immunologically distinct from cytoplasmic inclusions of neuronal intermediate filament inclusion disease
    Sabrina Mosaheb
    Electron Microscope Division, Sussex Centre for Advanced Microscopy, School of Life Sciences, University of Sussex, Brighton, UK
    Acta Neuropathol 110:360-8. 2005
    ..These observations indicate that abnormal protein aggregation follows separate pathways in different neuronal compartments of NIFID...
  50. pmc alpha-Internexin aggregates are abundant in neuronal intermediate filament inclusion disease (NIFID) but rare in other neurodegenerative diseases
    Nigel J Cairns
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce Street, Philadelphia, PA 19104 4283, USA
    Acta Neuropathol 108:213-23. 2004
    ..The discovery of alpha-internexin in neuronal cytoplasmic inclusions implicates novel mechanisms of pathogenesis in NIFID and other neurological diseases with pathological filamentous neuronal inclusions...
  51. ncbi request reprint Can alzheimer's disease and dementias with Lewy bodies be distinguished clinically?
    Myron F Weiner
    Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas 75390 9070, USA
    J Geriatr Psychiatry Neurol 16:245-50. 2003
    ..LB dementias differed from AD at initial evaluation, with more frequent hallucinations and delusions, EPSs, and seizures, and longitudinally in neuroleptic sensitivity, but the data did not distinguish LBV from DLBD...
  52. pmc Identification of a novel risk locus for progressive supranuclear palsy by a pooled genomewide scan of 500,288 single-nucleotide polymorphisms
    Stacey Melquist
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Am J Hum Genet 80:769-78. 2007
    ..Since DNA damage and lysosomal dysfunction have been implicated in aging and neurodegenerative processes, both genes are viable candidates for conferring risk of disease...