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Erschienen in: European Journal of Epidemiology 7/2018

27.06.2018 | COMMENTARY

Broadening the scope of epidemiologic dementia research

verfasst von: Sirwan K. L. Darweesh, Frank J. Wolters, M. Arfan Ikram, Daniel Bos, Albert Hofman

Erschienen in: European Journal of Epidemiology | Ausgabe 7/2018

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Excerpt

In this issue of EJE, Glymour and colleagues point out several shortcomings of the recently proposed NIA-AA framework of research criteria for diagnosing Alzheimer’s disease, in which Alzheimer’s disease is defined solely as a constellation of abnormal β-amyloid and pathologic tau deposits (Table 1) [1]. Glymour and colleagues emphasize that it remains uncertain whether β-amyloid causes Alzheimer’s disease, focusing specifically on the failure of numerous anti-amyloid trials, the observation that most individuals with cerebral β-amyloid plaques do not develop dementia (indicating low specificity for dementia), and the finding that there is no (or limited) evidence for β-amyloid in approximately one-quarter of individuals who meet clinical criteria for Alzheimer’s disease dementia (indicating low sensitivity). The authors further argue that it is unclear whether β-amyloid and tau reflect the most relevant biological processes leading to Alzheimer’s disease dementia.
Table 1
NIA-AA research framework for the diagnosis of Alzheimer’s disease: biomarker grouping
Category
Biomarker profile
Clinical signs or symptoms
Alzheimer’s disease
Presence of β-amyloid and tau; with or without neurodegeneration
May or may not be present
Alzheimer’s pathologic changes
Presence of β-amyloid; absence of tau; with neurodegeneration
Alzheimer’s and concomitant suspected non Alzheimer’s pathologic change
Presence of β-amyloid; absence of tau; without neurodegeneration
No Alzheimer’s disease
Absence of β-amyloid; with or without tau; with or without neurodegeneration
β-amyloid, Aggregated β-amyloid or associated pathologic state (i.e., cerebrospinal Aβ42 or Aβ42/Aβ40 ratio, or amyloid PET). Tau: Aggregated tau (neurofibrillary tangles) or associated pathologic state (i.e., cerebrospinal phosphorylated tau, or tau PET)
Literatur
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Zurück zum Zitat Neuropathology Group. Medical Research Council Cognitive F, Aging S. Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). Lancet (London, England). 2001;357(9251):169–75.CrossRef Neuropathology Group. Medical Research Council Cognitive F, Aging S. Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). Lancet (London, England). 2001;357(9251):169–75.CrossRef
20.
Zurück zum Zitat Association As. Alzheimer’s disease facts and figures. Alzheimer’s Dement. 2017;13(4):325–73.CrossRef Association As. Alzheimer’s disease facts and figures. Alzheimer’s Dement. 2017;13(4):325–73.CrossRef
Metadaten
Titel
Broadening the scope of epidemiologic dementia research
verfasst von
Sirwan K. L. Darweesh
Frank J. Wolters
M. Arfan Ikram
Daniel Bos
Albert Hofman
Publikationsdatum
27.06.2018
Verlag
Springer Netherlands
Erschienen in
European Journal of Epidemiology / Ausgabe 7/2018
Print ISSN: 0393-2990
Elektronische ISSN: 1573-7284
DOI
https://doi.org/10.1007/s10654-018-0421-9

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