Table 3.

Association between Aβ and gait

Study	Sample	Mean age	% Male	Methods	Gait parameters	Results
Buchman et al 2008 [62]	N=165 (59 with clinical AD diagnosis at death) community-dwelling adults	85 at baseline; 88 at death	44	AD pathology (tau & Aβ) at autopsy	Gait speed	AD pathology on autopsy associated with gait prior to death.
Buchman et al 2013 [63]	N=791 community-dwelling adults	82 at baseline; 89 at death	34	AD pathology (tau & Aβ) at autopsy	Gait speed	AD pathology on autopsy was associated with declining gait speed over an average of 6.4 years prior to death
del Campo et al 2015 [64]	N=128 non-demented community-dwelling adults	76	40	Cross-sectional; [18F]Florbetapir PET-measured Aβ	Gait speed	Greater Aβ deposition in the posterior and anterior putamen, caudate, semioval center, precuneus, anterior and posterior cingulate and occipital, temporal, and parietal lobes associated with slower gait speed
Wennberg et al, 2016 [66]	N=611 CN adults	63	51	Cross-sectional; PiB-PET SUVR	Gait speed, cadence, stride length, double support time, stance time variability	Greater PiB-PET SUVR in prefrontal, orbitofrontal, parietal, temporal, anterior cingulate, posterior cingulate/precuneus, and motor ROIs was associated with slower gait speed, lower cadence, longer double support time, and greater stance time variability. Results were independent of AD-associated neurodegeneration. In sex-stratified analyses, results were significant only among women.

AD, Alzheimer’s disease; SUVR, standardized uptake value ratio; CN, cognitively normal.