The MAPT H1 haplotype is associated with tangle-predominant dementia

[1]  W. Jagust,et al.  Discrepant diagnostic classification with AV45-PET and FDG-PET of clinically diagnosed Alzheimer's patients in the Alzheimer's Disease Neuroimaging Initiative , 2012, Alzheimer's & Dementia.

[2]  E. Junn,et al.  MicroRNAs in neurodegenerative diseases and their therapeutic potential. , 2012, Pharmacology & therapeutics.

[3]  J. Schneider,et al.  National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease , 2012, Alzheimer's & Dementia.

[4]  Sarah A. Chau,et al.  Current and Emerging Drug Treatment Options for Alzheimer’s Disease , 2011, Drugs.

[5]  R. Petersen,et al.  Neuropathologically defined subtypes of Alzheimer's disease with distinct clinical characteristics: a retrospective study , 2011, The Lancet Neurology.

[6]  A. Simon,et al.  Decrease in brain soluble amyloid precursor protein β (sAPPβ) in Alzheimer's disease cortex , 2011, Journal of neuroscience research.

[7]  J. Hardy,et al.  Disentangling the role of the tau gene locus in sporadic tauopathies. , 2010, Current Alzheimer research.

[8]  I. Mata,et al.  The Genetics of Parkinson Disease , 2010, Journal of geriatric psychiatry and neurology.

[9]  R. V. Van Heertum,et al.  Pittsburgh Compound B (11C-PIB) and Fluorodeoxyglucose (18 F-FDG) PET in Patients With Alzheimer Disease, Mild Cognitive Impairment, and Healthy Controls , 2010, Journal of geriatric psychiatry and neurology.

[10]  A. McKee,et al.  Mild traumatic brain injury: a risk factor for neurodegeneration , 2010, Alzheimer's Research & Therapy.

[11]  C. Jack,et al.  Update on the biomarker core of the Alzheimer's Disease Neuroimaging Initiative subjects , 2010, Alzheimer's & Dementia.

[12]  M. Owen,et al.  An association study of common variation at the MAPT locus with late‐onset Alzheimer's disease , 2009, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

[13]  Carol Brayne,et al.  Age, neuropathology, and dementia. , 2009, The New England journal of medicine.

[14]  Michael J. Owen,et al.  The effect of age and the H1c MAPT haplotype on MAPT expression in human brain , 2009, Neurobiology of Aging.

[15]  Charles D. Smith,et al.  Brains With Medial Temporal Lobe Neurofibrillary Tangles But No Neuritic Amyloid Plaques Are a Diagnostic Dilemma But May Have Pathogenetic Aspects Distinct From Alzheimer Disease , 2009, Journal of neuropathology and experimental neurology.

[16]  K. Marder,et al.  Association of glucocerebrosidase mutations with dementia with lewy bodies. , 2009, Archives of neurology.

[17]  E. Koo,et al.  Amyloid Precursor Protein Trafficking, Processing, and Function* , 2008, Journal of Biological Chemistry.

[18]  M. Tabaton,et al.  Evidence that the Amyloid beta Precursor Protein-intracellular domain lowers the stress threshold of neurons and has a "regulated" transcriptional role , 2008, Molecular Neurodegeneration.

[19]  Manuel A. R. Ferreira,et al.  PLINK: a tool set for whole-genome association and population-based linkage analyses. , 2007, American journal of human genetics.

[20]  J. Schneider,et al.  Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration , 2007, Acta Neuropathologica.

[21]  D. Selkoe,et al.  Aβ Oligomers – a decade of discovery , 2007, Journal of neurochemistry.

[22]  M. Spillantini,et al.  Frontotemporal Dementia with Tau Pathology , 2007, Neurodegenerative Diseases.

[23]  A. Myers,et al.  The MAPT H1c risk haplotype is associated with increased expression of tau and especially of 4 repeat containing transcripts , 2007, Neurobiology of Disease.

[24]  John X. Morris,et al.  The Fat of the Land: Do Agricultural Subsidies Foster Poor Health? , 2004, BMC Genetics.

[25]  K. Jellinger,et al.  Neurofibrillary tangle-predominant dementia: comparison with classical Alzheimer disease , 2007, Acta Neuropathologica.

[26]  T. Iwaki,et al.  Quantitative analysis of neurofibrillary pathology in a general population to reappraise neuropathological criteria for senile dementia of the neurofibrillary tangle type (tangle‐only dementia): The Hisayama study , 2006, Neuropathology : official journal of the Japanese Society of Neuropathology.

[27]  H. Akiyama,et al.  Immunohistochemical investigation of neurofibrillary tangles and their tau isoforms in brains of limbic neurofibrillary tangle dementia , 2006, Neuroscience Letters.

[28]  T. Sacktor,et al.  Atypical Protein Kinase C in Neurodegenerative Disease I: PKM&zgr; Aggregates With Limbic Neurofibrillary Tangles and AMPA Receptors in Alzheimer Disease , 2006, Journal of neuropathology and experimental neurology.

[29]  N. Ghebranious,et al.  Detection of ApoE E2, E3 and E4 alleles using MALDI-TOF mass spectrometry and the homogeneous mass-extend technology , 2005, Nucleic acids research.

[30]  A M Pittman,et al.  The H1c haplotype at the MAPT locus is associated with Alzheimer's disease. , 2005, Human molecular genetics.

[31]  A J Lees,et al.  Linkage disequilibrium fine mapping and haplotype association analysis of the tau gene in progressive supranuclear palsy and corticobasal degeneration , 2005, Journal of Medical Genetics.

[32]  H. Stefánsson,et al.  A common inversion under selection in Europeans , 2005, Nature Genetics.

[33]  A. Andreadis.  Tau gene alternative splicing: expression patterns, regulation and modulation of function in normal brain and neurodegenerative diseases. , 2005, Biochimica et biophysica acta.

[34]  C. DeCarli,et al.  Neutralization of Transthyretin Reverses the Neuroprotective Effects of Secreted Amyloid Precursor Protein (APP) in APPSw Mice Resulting in Tau Phosphorylation and Loss of Hippocampal Neurons: Support for the Amyloid Hypothesis , 2004, The Journal of Neuroscience.

[35]  M. Yamada.  Senile dementia of the neurofibrillary tangle type (tangle‐only dementia): Neuropathological criteria and clinical guidelines for diagnosis * , 2003, Neuropathology : official journal of the Japanese Society of Neuropathology.

[36]  J. Hardy,et al.  The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .

[37]  R. Mohs,et al.  Consortium to establish a registry for Alzheimer's disease (CERAD) clinical and neuropsychological assessment of Alzheimer's disease. , 2002, Psychopharmacology bulletin.

[38]  D. Dickson,et al.  Morphological and Biochemical Correlations of Abnormal Tau Filaments in Progressive Supranuclear Palsy , 2002, Journal of neuropathology and experimental neurology.

[39]  L. Behar,et al.  Axonal Tau mRNA Localization Coincides with Tau Protein in Living Neuronal Cells and Depends on Axonal Targeting Signal , 2001, The Journal of Neuroscience.

[40]  K. Blennow,et al.  Reduced Expression of Amyloid Precursor Protein, Presenilin-1 and rab3a in Cortical Brain Regions in Alzheimer’s Disease , 2001, Dementia and Geriatric Cognitive Disorders.

[41]  E. Otomo,et al.  Senile Dementia of the Neurofibrillary Tangle Type: A Comparison with Alzheimer’s Disease , 2001, Dementia and Geriatric Cognitive Disorders.

[42]  M. Tabaton,et al.  Corticobasal degeneration shares a common genetic background with progressive supranuclear palsy , 2000, Annals of neurology.

[43]  R. Marx,et al.  Identification of 3′UTR region implicated in tau mRNA stabilization in neuronal cells , 1999, Journal of Molecular Neuroscience.

[44]  I Litvan,et al.  Association of an extended haplotype in the tau gene with progressive supranuclear palsy. , 1999, Human molecular genetics.

[45]  J. Morris,et al.  Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease , 1999, Annals of neurology.

[46]  Masanori Kato,et al.  Clinical Aspects of ‘Senile Dementia of the Tangle Type’ – A Subset of Dementia in the Senium Separable from Late-Onset Alzheimer’s Disease , 1998, Dementia and Geriatric Cognitive Disorders.

[47]  K. Jellinger,et al.  Senile Dementia with Tangles (Tangle Predominant Form of Senile Dementia) , 1998, Brain pathology.

[48]  J Bohl,et al.  Staging of Alzheimer-Related Cortical Destruction , 1997, International Psychogeriatrics.

[49]  H. Akiyama,et al.  A subset of senile dementia with high incidence of the apolipoprotein E ϵ2 allele , 1997 .

[50]  J. Morris,et al.  The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part XIII. , 1996, Neurology.

[51]  J. Morrison,et al.  Regional distribution of neurofibrillary tangles and senile plaques in the cerebral cortex of elderly patients: a quantitative evaluation of a one-year autopsy population from a geriatric hospital. , 1994, Cerebral cortex.

[52]  J. Wall,et al.  Mass and physical dimensions of two distinct populations of paired helical filaments , 1994, Neurobiology of Aging.

[53]  V. Ambros,et al.  The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14 , 1993, Cell.

[54]  J. Haines,et al.  Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. , 1993, Science.

[55]  P. Lansbury,et al.  The carboxy terminus of the beta amyloid protein is critical for the seeding of amyloid formation: implications for the pathogenesis of Alzheimer's disease. , 1993, Biochemistry.

[56]  M. Mattson,et al.  Evidence for excitoprotective and intraneuronal calcium-regulating roles for secreted forms of the β-amyloid precursor protein , 1993, Neuron.

[57]  J. Rowe,et al.  Human aging: usual and successful. , 1987, Science.

[58]  H. Horvitz,et al.  The lin-14 locus of Caenorhabditis elegans controls the time of expression of specific postembryonic developmental events. , 1987, Genes & development.

[59]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[60]  M. Kidd.  Paired Helical Filaments in Electron Microscopy of Alzheimer's Disease , 1963, Nature.

[61]  Charles Duyckaerts,et al.  National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach , 2011, Acta Neuropathologica.

[62]  S. Schmidt,et al.  Tissue processing prior to protein analysis and amyloid-beta quantitation. , 2005, Methods in molecular biology.

[63]  S. Schmidt,et al.  Tissue Processing Prior to Protein Analysis and Amyloid-ß Quantitation , 2005 .

[64]  H. Braak,et al.  Neuropathological stageing of Alzheimer-related changes , 2004, Acta Neuropathologica.

[65]  K. Jellinger,et al.  Neurofibrillary tangle predominant form of senile dementia of Alzheimer type: a rare subtype in very old subjects , 2004, Acta Neuropathologica.

[66]  H. Akiyama,et al.  A subset of senile dementia with high incidence of the apolipoprotein E epsilon2 allele. , 1997, Annals of neurology.

[67]  K. Iqbal,et al.  Alzheimer's disease : biology, diagnosis, and therapeutics , 1996 .

[68]  M A Pericak-Vance,et al.  Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease. , 1993, Neurology.

[69]  J. Ulrich.  Abundant neurofibrillary tangles without senile plaques in a subset of patients with senile dementia , 1992 .