We examined inter-relationships among various neurodegeneration biomarkers and cognitive and physical impairment in the presence or absence of amyloid pathology.

In participants in the Wake Forest Alzheimer’s Disease Research Center Clinical Core cohort, we examined cross-sectional associations among MRI neurodegeneration measures (parietal and temporal cortical thickness, and hippocampal volume; n=520), β-amyloid deposition (PiB SUVR) and positivity (Aβ+; PiB SUVR≥1.21) on PET (n=126), cognitive status (normal/cognitively impaired), and physical function (4m-walk gait speed). Cognitive impairment was determined via expert consensus review; gait speed was median-split to define better or worse motor function. Unadjusted models are presented.

Across all participants we found strong correlations among neurodegeneration measures; if hippocampal volume, temporal thickness, or parietal thickness were lower, the other two were also significantly likely to be lower (n=520, r’s>0.35, p’s<0.01). Elevated Aβ (PiB SUVR) was also significantly associated with neurodegeneration measures (n=126, |r|’s>0.26, p’s<0.01).

Lower hippocampal volume was related to cognitive impairment among Aβ+ (n=47, t=4.2, p=0.0002), but not among Aβ- (n=83; p=0.13) participants. Hippocampal volume did not predict motor impairment regardless of Aβ status. No association was seen between temporal or parietal thickness and cognitive impairment in Aβ+ participants; however, in Aβ- participants, there was an association between lower parietal thickness and cognitive impairment (n=83, t=2.4, p=0.02). Temporal and parietal thicknesses were related to motor impairment in Aβ- (p<0.01) but not Aβ+ participants.

These results suggest that, in our community-dwelling cohort, associations among neurodegeneration measures and cognitive/motor function differ based on Aβ burden. Reduced temporal and parietal cortical thickness may predict cognitive and motor impairment better among Aβ- rather than Aβ+ participants.