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lüll Beta-amyloid deposition and the aging brain Rodrigue KM; Kennedy KM; Park DCNeuropsychol Rev 2009[Dec]; 19 (4): 436-50A central issue in cognitive neuroscience of aging research is pinpointing precise neural mechanisms that determine cognitive outcome in late adulthood as well as identifying early markers of less successful cognitive aging. One promising biomarker is beta amyloid (Abeta) deposition. Several new radiotracers have been developed that bind to fibrillar Abeta providing sensitive estimates of amyloid deposition in various brain regions. Abeta imaging has been primarily used to study patients with Alzheimer's Disease (AD) and individuals with Mild Cognitive Impairment (MCI); however, there is now building data on Abeta deposition in healthy controls that suggest at least 20% and perhaps as much as a third of healthy older adults show significant deposition. Considerable evidence suggests amyloid deposition precedes declines in cognition and may be the initiator in a cascade of events that indirectly leads to age-related cognitive decline. We review studies of Abeta deposition imaging in AD, MCI, and normal adults, its cognitive consequences, and the role of genetic risk and cognitive reserve.|Aging/genetics/*metabolism[MESH]|Amyloid beta-Peptides/genetics/*metabolism[MESH]|Brain/*metabolism[MESH]|Cognition Disorders/genetics/metabolism[MESH]|Genetic Predisposition to Disease[MESH]|Humans[MESH]|Models, Neurological[MESH]|Plaque, Amyloid/genetics/*metabolism[MESH] |