Imaging tau and amyloid-β proteinopathies in Alzheimer disease and other conditions.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing literature on PET imaging of amyloid and tau without systematic review methodology.
PubMed 29449700 · doi:10.1038/nrneurol.2018.9
What was done
This narrative review synthesized literature on in vivo positron emission tomography (PET) imaging of extracellular amyloid-β (Aβ) and intracellular tau neurofibrillary tangles in Alzheimer disease (AD) and related neurodegenerative conditions. It discussed the clinical and clinical trial utility of approved Aβ-PET tracers for patient stratification and outcome tracking, the development of selective tau-PET tracers, and the utility of longitudinal multimodal imaging to characterize disease progression and cognitive decline.
What was found
The abstract reports no quantitative results, sensitivity/specificity values, or statistical metrics. Qualitatively, it highlights that Aβ deposition is a protracted process that begins more than two decades before the onset of clinical symptoms, and that concurrent longitudinal Aβ and tau imaging can clarify whether these pathological processes exert independent, sequential, or synergistic effects on neurodegeneration and cognitive impairment.
Why it matters
In vivo molecular imaging enables tracking of AD neuropathology before and during clinical manifestation. Understanding how Aβ and tau accumulate and interact over time is essential for optimizing patient selection and monitoring target engagement in clinical trials of disease-modifying therapies.
Limits
This is an unsystematic narrative review, not an empirical study or meta-analysis. No sample sizes, search criteria, diagnostic accuracy metrics, or quantitative effect sizes are provided in the abstract.
Cited by
- supports Virtually all neurodegenerative diseases feature the aggregation of abnormal protein clumps either inside neurons or in the extracellular spaces between neurons.