Published in:
01-07-2018 | COMMENTARY
Broadening the scope of epidemiologic dementia research
Published in: European Journal of Epidemiology | Issue 7/2018
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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
|