Beta-amyloid (Ab) plaques have been well-documented in the brains of persons with Alzheimer’s disease. The
precise effect of this deposition on the disruption of human brain function/structure is unclear. Notably, how this
protein accumulation is related to the course of normal aging is unknown. Approximately a third of older adults
have levels of amyloid on par with those individuals diagnosed with AD, yet are cognitively normal. Examining the
time-course of Aβ deposition and its neural and cognitive consequences in normal and healthy aging populations
is an important step in disentangling healthy from pathological aging. Our goal is to characterize the distribution
of Aβ in a normally aging population across the adult lifespan.
The Dallas Lifespan Brain Study (DLBS) is an ongoing large study of brain structural and functional aging and the
impact on cognitive performance that will enroll 350 individuals aged 20-89 (n = 50 per decade). We are now PET
scanning a subset of these individuals (n = 260) to quantify amyloid deposition using AV-45 (18F-florpiramine). To
date, we have scanned 50 individuals ranging in age from 45-89 (m = 63.95; 20 men, 37 women) with a mean
education level of 16.18 years (range = 12-21) and MMSE = 29 (26-30). The ultimate goal of the study is to not
only characterize when in the age span beta-amyloid deposition begins to occur but also to examine if earlier
deposition in middle-age is associated with brain structural decline (e.g., regional volumes, white matter integrity)
and age-related differences in patterns of functional neural activation, as well as cognitive performance. We expect
that the DLBS will greatly expand the existing knowledge of the time course and neural/cognitive consequences
of amyloid deposition in normal aging. We will report the DLBS amyloid findings to date.
