We used longitudinal CSF data on β-amyloid42 (Aβ42) to identify cognitively healthy people who declined in CSF Aβ42 over time, indicating possible accumulation of β-amyloid pathology in the brain parenchyma. We then compared brain structures between people who had normal CSF Aβ42 levels at baseline and follow, people who started with normal CSF Aβ42 levels but who declined during the study, and people who had a positive CSF Aβ42 profile (reduced levels) already at baseline.
We found increased atrophy rates in people with declining CSF Aβ42 levels, suggesting that the accumulation of β-amyloid was coupled to increased atrophy rates. Surprisingly, the increased atrophy rates were not particularly pronounced in the temporal cortex or the hippocampus, which are believed to be early engaged in Alzheimer's disease. Instead, atrophy rates were increased in fronto-parietal cortical regions. These are areas where β-amyloid pathology is known to accumulate early, perhaps suggesting that the emerging β-amyloid pathology was coupled to local neurotoxicity.
AlzForum wrote about a story about the study here and MedicalResearch.com wrote about it here.
