Early Neuroinflammation in Down Syndrome May Contribute to Higher Alzheimer’s Disease Risk

Recent research from the University of São Paulo (USP) in Brazil sheds light on the early brain changes in people with Down syndrome that may explain their heightened risk of developing Alzheimer’s disease. The study highlights significant neuroinflammation occurring in young individuals with Down syndrome, as early as their 20s, which appears to be closely linked to the accumulation of beta-amyloid plaques—protein deposits associated with Alzheimer’s pathology.

Down syndrome is known for causing accelerated aging, where up to 90% of individuals may develop Alzheimer’s disease by age 70. This is largely attributed to the presence of an extra copy of chromosome 21, which includes the amyloid precursor protein (APP) gene. Overexpression of this gene leads to increased production of beta-amyloid peptides, forming plaques that disrupt neural communication and trigger inflammatory responses.

The groundbreaking aspect of this study is the mapping of neuroinflammatory processes in living brains using nuclear medicine techniques, specifically positron emission tomography (PET). This imaging method allowed researchers to observe inflammations and beta-amyloid deposits in regions such as the frontal, temporal, occipital, and limbic areas. The findings reveal that neuroinflammation begins early, well before significant plaque formation, suggesting it may be a precursor to Alzheimer’s pathology.

Furthermore, the study found a strong correlation between the degree of neuroinflammation and beta-amyloid accumulation, especially in adults over 50. To deepen their understanding, scientists studied genetically modified mice that mimic Down syndrome, monitoring disease progression over two years. These animal models provided valuable insights into how neuroinflammation evolves and contributes to neural decline.

The research also described a biphasic pattern of neuroinflammation. Initially, microglia, the brain’s innate immune cells, act protectively. Over time, this response shifts to a pro-inflammatory state that can exacerbate neuronal damage. This suggests that targeting neuroinflammation could be a promising strategy for slowing the disease’s progression.

By establishing that neuroinflammation happens early and is linked to later plaque buildup, the study offers new avenues for intervention. Therapies aimed at reducing brain inflammation might delay or prevent the onset of Alzheimer’s in people with Down syndrome. Additionally, the use of advanced imaging tools enables real-time monitoring of inflammatory processes, paving the way for personalized treatment plans and inclusion of this population in Alzheimer’s clinical trials.

This research emphasizes the importance of early detection and intervention, with the potential to significantly modify the trajectory of Alzheimer’s disease in individuals with Down syndrome, who represent a unique and vulnerable population. These findings are a crucial step towards safer, more effective therapies tailored to their needs.

Source: https://medicalxpress.com/news/2025-10-early-neuroinflammation-people-syndrome-high.html