The increasing prevalence of dementia causes a substantial burden on the health care system. The modification of risk factors in individuals at risk of cognitive decline could curb the dementia epidemic, as first shown by a Finnish intervention study to prevent cognitive decline and disability (FINGER).1 This study found that a multimodal lifestyle intervention is beneficial for the maintenance of cognitive functioning in individuals at high risk of cognitive decline based on cardiovascular risk factors. Earlier neuroimaging research in the FINGER sample has found an association between early brain β-amyloid accumulation and decline in cognitive functions.2 Here, we aimed to characterize the associations between brain β-amyloid and regional brain volumes in individuals at increased risk of cognitive decline. To this end, we studied a sample of elderly subjects who had participated in the FINGER study by using MRI and PET with 11C-labeled-Pittsburgh compound-B (11C PIB), a radioligand selective for β-amyloid plaques.
We found that in subjects with early signs of brain β-amyloid deposition, the increases in 11C PIB uptake were associated with smaller gray matter volumes in the temporal lobe, including the hippocampus, and in the prefrontal lobe. This finding suggests that β-amyloid may incite neurodegeneration even before clinical symptoms emerge. Because the regions displaying smaller gray matter volumes in association with β-amyloid deposition included parts of the medial temporal lobe memory system, it is possible that these reductions in gray matter volumes have an impact on later cognitive decline.