Tau positron emission tomography (PET) or [18F]flortaucipir appears to be more sensitive than cortical thickness measurements and β-amyloid (Aβ) PET ([18F] flutemetamol) to detect early cognitive changes in preclinical Alzheimer disease (AD), according to study results published in Neurology.
A subset population of the Swedish Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably (BioFINDER) study was composed of 106 participants with preclinical AD (Aβ-positive cognitively normal individuals; n=33), prodromal AD (Aβ-positive mild cognitive impairment; n=25), and probable AD dementia (n=48). All participants underwent structural magnetic resonance imaging measurements and tau PET. In addition, 88 patients underwent Aβ PET. In adjusted analyses, the researchers evaluated the associations among 7 regions of interest (ie, medial and lateral parietal cortex, medial and lateral temporal cortex, frontal cortex, occipital cortex, and a whole-brain composite) and neuropsychological tests for all assessed imaging modalities.
[18F]flortaucipir was associated with reduced global cognition, processing speed, and memory in preclinical AD (range standardized β 0.35-0.52; P <.05 uncorrected for multiple comparisons). No such association was found with [18F]flutemetamol. Increased uptake of [18F]flortaucipir and reduced cortical thickness were also associated with worse performance on the naming condition of the Alzheimer Disease Assessment Scale in the left temporoparietal cortex in the combined prodromal AD and AD dementia group. In addition, increased uptake of [18F]flutemetamol uptake was associated with lower delayed recall memory task scores (P <.05 uncorrected for multiple comparisons). Associations between [18F]flortaucipir and cortical thickness with cognitive scores were strongest in the lateral and medial parietal cortex and in the lateral temporal cortex.
The lack of assessment for all cognitive domains, the small sample size, and the cross-sectional nature of the data analysis represented potential limitations of the findings.
Future work in “identifying the contribution of these neurobiological hallmarks of AD to cognitive changes could eventually improve the diagnostic and prognostic process in AD and may inform design, participant selection, and monitoring of clinical trials,” the researchers concluded.
Ossenkoppele R, Smith R, Ohlsson T, et al. Associations between tau, Aβ, and cortical thickness with cognition in Alzheimer disease. Neurology. 2019;92(6):e601-e612.
This article originally appeared on Neurology Advisor