1. Cerebrospinal fluid biomarkers and cerebral atrophy in distinct clinical variants of probable Alzheimer's disease.

    Neurobiology of Aging 36(8):2340 (2015) PMID 25990306 PMCID PMC4465267

    Different clinical variants of probable Alzheimer's disease (AD) share underlying plaques and tangles but show distinct atrophy patterns. We included 52 posterior cortical atrophy, 29 logopenic variant primary progressive aphasia, 53 early-onset and 42 late-onset AD patients, selected for abnorm...
  2. Existing Pittsburgh Compound-B positron emission tomography thresholds are too high: statistical and pathological evaluation.

    Brain 138(Pt 7):2020 (2015) PMID 25953778

    Amyloid-β, a hallmark of Alzheimer's disease, begins accumulating up to two decades before the onset of dementia, and can be detected in vivo applying amyloid-β positron emission tomography tracers such as carbon-11-labelled Pittsburgh compound-B. A variety of thresholds have been applied in the...
  3. Executive dysfunction.

    Continuum: Lifelong Learning in Neurology 21(3 Behavioral Neurology and Neuropsychiatry):646 (2015) PMID 26039846

    Executive functions represent a constellation of cognitive abilities that drive goal-oriented behavior and are critical to the ability to adapt to an ever-changing world. This article provides a clinically oriented approach to classifying, localizing, diagnosing, and treating disorders of execut...
  4. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis.
    Willemijn Jansen, Rik Ossenkoppele, Dirk L Knol, Betty M Tijms, Philip Scheltens, Frans R J Verhey, Pieter Jelle Visser, Pauline Aalten, Dag Aarsland, Daniel Alcolea, Myriam Alexander, Ina S Almdahl, Steven E Arnold, Inês Baldeiras, Henryk Barthel, Bart N M van Berckel, Kristen Bibeau, Kaj Blennow, David J Brooks, Mark A van Buchem, Vincent Camus, Enrica Cavedo, Kewei Chen, Gael Chetelat, Ann D Cohen, Alexander Drzezga, Sebastiaan Engelborghs, Anne M Fagan, Tormod Fladby, Adam S Fleisher, Wiesje M van der Flier, Lisa Ford, Stefan Förster, Juan Fortea, Nadia Foskett, Kristian S Frederiksen, Yvonne Freund-Levi, Giovanni B Frisoni, Lutz Froelich, Tomasz Gabryelewicz, Kiran Dip Gill, Olymbia Gkatzima, Estrella Gómez-Tortosa, Mark Forrest Gordon, Timo Grimmer, Harald Hampel, Lucrezia Hausner, Sabine Hellwig, Sanna-Kaisa Herukka, Helmut Hildebrandt, Lianna Ishihara, Adrian Ivanoiu, William Jagust, Peter Johannsen, Ramesh Kandimalla, Elisabeth Kapaki, Aleksandra Klimkowicz-Mrowiec, William E Klunk, Sebastian Köhler, Norman Koglin, Johannes Kornhuber, Milica G Kramberger, Koen Van Laere, Susan M Landau, Dong Young Lee, Mony de Leon, Viviana Lisetti, Alberto Lleó, Karine Madsen, Wolfgang Maier, Jan Marcusson, Niklas Mattsson, Alexandre de Mendonça, Olga Meulenbroek, Philipp T Meyer, Mark A Mintun, Vincent Mok, José Luis Molinuevo, Hanne Møllergård, John C Morris, Barbara Mroczko, Stefan Van der Mussele, Duk L Na, Andrew Newberg, Agneta Nordberg, Arto Nordlund, Gerald P Novak, George Paraskevas, Lucilla Parnetti, Gayan Perera, Oliver Peters, Julius Popp, Sudesh Prabhakar, Gil D Rabinovici, Inez H G B Ramakers, Lorena Rami, Catarina Resende de Oliveira, Juha O Rinne, Karen M Rodrigue, Eloy, Catherine M Roe, Uros Rot, Christopher Rowe, Eckart Rüther, Osama Sabri, Páscual Sanchez-Juan, Isabel Santana, Marie Sarazin, Johannes Schröder, Christin Schütte, Sang W Seo, Femke Soetewey, Hilkka Soininen, Luiza Spiru, Hanne Struyfs, Charlotte E Teunissen, Magda Tsolaki, Rik Vandenberghe, Marcel Verbeek, Victor L Villemagne, Stephanie J B Vos, Linda J C van Waalwijk Doorn, Gunhild Waldemar, Anders Wallin, Åsa K Wallin, Jens Wiltfang, David A Wolk, Marzena Zboch, and Henrik Zetterberg

    JAMA 313(19):1924 (2015) PMID 25988462 PMCID PMC4486209

    Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies. To use in...
  5. Prevalence of amyloid PET positivity in dementia syndromes: a meta-analysis.

    JAMA 313(19):1939 (2015) PMID 25988463 PMCID PMC4517678

    Amyloid-β positron emission tomography (PET) imaging allows in vivo detection of fibrillar plaques, a core neuropathological feature of Alzheimer disease (AD). Its diagnostic utility is still unclear because amyloid plaques also occur in patients with non-AD dementia. To use individual participa...
  6. Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy.

    Journal of Neurology, Neurosurgery & Psychiatry 86(3):244 (2015) PMID 24899730 PMCID PMC4256124

    Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. However, previous studies have failed to detect alterations of τ species in other primary tauopathies. We assessed CSF τ protein abnormalities in ...
  7. Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy.

    Journal of Neurology, Neurosurgery & Psychiatry 86(3):244 (2015) PMID 24899730

    Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. However, previous studies have failed to detect alterations of τ species in other primary tauopathies. We assessed CSF τ protein abnormalities in ...
  8. Clinical Use of Amyloid PET Neuroimaging: Practical and Bioethical Considerations

    American Journal of Geriatric Psychiatry 23(3):S150 (2015)

  9. The Translational Journey of Brain β-Amyloid Imaging: From Positron Emission Tomography to Autopsy to Clinic.

    JAMA Neurology 72(3):265 (2015) PMID 25621934

  10. Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy.

    Journal of Neurology, Neurosurgery & Psychiatry 86(3):244 (2015) PMID 24899730 PMCID PMC4256124

    Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. However, previous studies have failed to detect alterations of τ species in other primary tauopathies. We assessed CSF τ protein abnormalities in ...
  11. The Translational Journey of Brain β-Amyloid Imaging: From Positron Emission Tomography to Autopsy to Clinic.

    JAMA Neurology 72(3):265 (2015) PMID 25621934

  12. Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy.

    Journal of Neurology, Neurosurgery & Psychiatry 86(3):244 (2015) PMID 24899730 PMCID PMC4256124

    Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. However, previous studies have failed to detect alterations of τ species in other primary tauopathies. We assessed CSF τ protein abnormalities in ...
  13. Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy.

    Journal of Neurology, Neurosurgery & Psychiatry 86(3):244 (2015) PMID 24899730 PMCID PMC4256124

    Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. However, previous studies have failed to detect alterations of τ species in other primary tauopathies. We assessed CSF τ protein abnormalities in ...
  14. Divergent CSF τ alterations in two common tauopathies: Alzheimer's disease and progressive supranuclear palsy.

    Journal of Neurology, Neurosurgery & Psychiatry 86(3):244 (2015) PMID 24899730 PMCID PMC4256124

    Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. However, previous studies have failed to detect alterations of τ species in other primary tauopathies. We assessed CSF τ protein abnormalities in ...
  15. Prodromal posterior cortical atrophy: clinical, neuropsychological, and radiological correlation.

    Neurocase 21(1):44 (2015) PMID 24308559

    We present longitudinal clinical, cognitive, and neuroimaging data from a 63-year-old woman who enrolled in research as a normal control and evolved posterior cortical atrophy (PCA) over 5 year follow-up. At baseline she reported only subtle difficulty driving and performed normally on cognitive...
  16. Prodromal posterior cortical atrophy: clinical, neuropsychological, and radiological correlation.

    Neurocase 21(1):44 (2015) PMID 24308559 PMCID PMC4318700

    We present longitudinal clinical, cognitive, and neuroimaging data from a 63-year-old woman who enrolled in research as a normal control and evolved posterior cortical atrophy (PCA) over 5 year follow-up. At baseline she reported only subtle difficulty driving and performed normally on cognitive...
  17. Prodromal posterior cortical atrophy: clinical, neuropsychological, and radiological correlation.

    Neurocase 21(1):44 (2015) PMID 24308559 PMCID PMC4318700

    We present longitudinal clinical, cognitive, and neuroimaging data from a 63-year-old woman who enrolled in research as a normal control and evolved posterior cortical atrophy (PCA) over 5 year follow-up. At baseline she reported only subtle difficulty driving and performed normally on cognitive...
  18. Prodromal posterior cortical atrophy: clinical, neuropsychological, and radiological correlation.

    Neurocase 21(1):44 (2015) PMID 24308559

    We present longitudinal clinical, cognitive, and neuroimaging data from a 63-year-old woman who enrolled in research as a normal control and evolved posterior cortical atrophy (PCA) over 5 year follow-up. At baseline she reported only subtle difficulty driving and performed normally on cognitive...
  19. Tau, amyloid, and hypometabolism in a patient with posterior cortical atrophy.

    Annals of Neurology 77(2):338 (2015) PMID 25448043

    Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. We report a patient with posterior cortical atrophy (visual variant of Alzh...
  20. Tau, amyloid, and hypometabolism in a patient with posterior cortical atrophy.

    Annals of Neurology 77(2):338 (2015) PMID 25448043 PMCID PMC4382124

    Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. We report a patient with posterior cortical atrophy (visual variant of Alzh...