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. 2018 Aug;24(7):693-702.
doi: 10.1017/S135561771800022X. Epub 2018 Apr 30.

Neuropsychological Profiles and Trajectories in Preclinical Alzheimer's Disease

Jean K Ho  1 , Daniel A Nation  1 ; Alzheimer’s Disease Neuroimaging Initiative
Affiliations

Neuropsychological Profiles and Trajectories in Preclinical Alzheimer's Disease

Jean K Ho et al. J Int Neuropsychol Soc. 2018 Aug.

Abstract

Objectives: The present study investigated the independent and synergistic effects of amyloid beta (Aβ1-42) and phosphorylated tau (Ptau) pathologies on neuropsychological profiles and trajectories in cognitively normal older adults.

Methods: Alzheimer's Disease Neuroimaging Initiative participants identified as cognitively normal at baseline underwent longitudinal assessment (N=518; 0, 12, 24, 36 months), baseline lumbar puncture and follow-up cognitive exams. Cerebral spinal fluid (CSF) biomarker profiles (Aβ-Ptau-, Aβ+Ptau-, Aβ-Ptau+, Aβ+Ptau+) were compared on baseline profiles and trajectories for memory (Rey Auditory Verbal Learning Test), attention/executive function (Trail Making Test, A and B), language (Animal Fluency, Vegetable Fluency, Boston Naming Test) and processing speed (Digit Symbol) using multilevel models.

Results: The Aβ+Ptau+ group exhibited significantly worse baseline performance on tests of memory and executive function relative to the Aβ-Ptau+ and Aβ-Ptau- groups. The Aβ+Ptau- group fell between the Aβ+Ptau+ participants and the Aβ-Ptau- and Aβ-Ptau+ groups on all three cognitive domains and exhibited worse baseline executive function. The Aβ-Ptau+ group performed worse than Aβ-Ptau- participants on processing speed. Over 36-month follow-up, the Aβ+Ptau+ group exhibited the greatest declines in memory and semantic fluency compared to all other groups.

Conclusions: Cognitively normal older adults with both Aβ and Ptau pathology exhibited the weakest profile, marked by the worst memory decline compared to the other groups. Other subtle changes in this group included declines in executive function and semantic fluency. Those with Ptau pathology alone showed slowed processing speed, and those with Aβ pathology alone showed worse attention and executive function compared to biomarker negative participants. (JINS, 2018, 24, 693-702).

Keywords: Alzheimer’s disease; Amyloid beta; Biomarkers; Cognition; Memory; Tau.

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Conflict of interest statement

Conflict of Interest: None.

Figures

Figure 1
Figure 1
The Aβ+Ptau+ participants showed greater decline in immediate memory relative to all other groups over follow-up: the Aβ+Ptau− group (p = .002), the Aβ−Ptau+ group (p = .004), and the Aβ−Ptau− group (p < .002).
Figure 2
Figure 2
The Aβ+Ptau+ participants showed greater decline in delayed memory relative to all other groups over follow-up: the Aβ+Ptau− group (p = .02), the Aβ−Ptau+ group (p = .01), and the Aβ−Ptau− group (p < .0005).
Figure 3
Figure 3
The Aβ+Ptau+ participants showed greater decline in recognition memory relative to all other groups over follow-up: the Aβ+Ptau− group (p = .0006), the Aβ−Ptau+ and the Aβ−Ptau− group (p < .0001).
Figure 4
Figure 4
The Aβ+Ptau+ participants showed greater decline in executive function relative to the Aβ−Ptau− group over follow-up (p = .0008). Scores are inverted such that higher values indicate better performance.
Figure 5
Figure 5
The Aβ+Ptau+ participants showed greater decline in semantic fluency relative to relative to all other groups over follow-up: the Aβ+Ptau− group (p = .003), the Aβ−Ptau+ group (p = .05), and the Aβ−Ptau− group (p = .004).
See this image and copyright information in PMC

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