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Alzheimer's Protein Causes Early Brain Shrinkage, Study Finds
Researchers have identified a direct connection between high levels of amyloid-beta protein and early brain shrinkage in Alzheimer's patients. Their study focused on significant volume loss in the basal forebrain and hippocampus, key regions involved in memory and cognitive function.
Amyloid-beta, a peptide known to accumulate in the brain, forms plaques that interfere with neuron communication and lead to their death. These plaques are a hallmark of Alzheimer's disease, contributing to the progressive decline in cognitive functions, PsyPost reported.
Over time, amyloid-beta accumulation hampers neurons' ability to form new connections, crucial for learning and memory, thus resulting in brain shrinkage.
Led by Ying Xia, the research team sought to investigate the extent of volume loss in the basal forebrain and hippocampus among older adults with varying levels of amyloid-beta.
The study involved 516 participants aged 60 years or older from the Australian Imaging, Biomarker, and Lifestyle (AIBL) study of aging. At the outset, 40 participants had Alzheimer's disease, 62 had mild cognitive impairment, and 414 had no cognitive impairments.
The participants underwent positron emission tomography (PET) imaging to assess amyloid-beta levels and magnetic resonance imaging (MRI) to measure brain volumes. Cognitive assessments were also conducted.
They were followed for up to 14 years, with an average follow-up of five years. During this period, participants completed multiple MRIs to monitor brain volume changes.
At the beginning of the study, participants were classified based on cognitive status and amyloid-beta levels. Findings revealed that individuals with cognitive impairments and high amyloid-beta levels had smaller basal forebrain and hippocampus volumes from the start.
Over time, these regions in participants with high amyloid-beta levels exhibited faster volume loss compared to those with lower levels.
"These findings strongly support the early and substantial vulnerability of the BF [basal forebrain region] and further reveal the distinctive degeneration of BF subregions in normal aging and AD [Alzheimer's disease]," the authors concluded.
The study published in the journal Neurobiology of Aging shows the critical link between amyloid-beta levels and accelerated brain shrinkage with aging. However, the authors caution that the study's participants were generally well-educated, scored high on cognitive tests, and had few additional medical conditions, indicating that results might vary in a more representative population.
This research provides valuable insights into the early stages of Alzheimer's disease, highlighting the importance of monitoring amyloid-beta levels for early intervention and potential treatment strategies.
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