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Study Links Neuroinflammation to Dementia Risk in Parkinson’s Disease

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A recent study has shed light on the mechanisms behind the development of dementia in Parkinson’s disease (PD), identifying significant neuroinflammation as a potential early indicator. The study was published in the journal Brain, offers critical insights that could lead to improved therapeutic strategies.

Dementia is one of the most debilitating aspects of Parkinson’s disease, with nearly half of all patients developing it within ten years of diagnosis. The NET-PDD study aims to understand why some individuals with PD develop dementia early while others remain cognitively intact. The research focuses on two key processes: neuroinflammation and tau protein accumulation, both implicated in various neurodegenerative disorders.

The study involved 36 newly diagnosed PD patients and 20 age-matched controls. The patients were stratified into high and low dementia risk groups based on specific predictors such as impaired pentagon copying, semantic fluency performance, and the MAPT H1/H1 genotype. This stratification was designed to identify individuals at higher risk of developing dementia early in their disease course.

The NET-PDD study utilised positron emission tomography (PET) imaging with two tracers: 11C-PK11195 to index neuroinflammation and 18F-AV-1451 for misfolded tau. The results revealed significantly elevated neuroinflammation in multiple subcortical and restricted cortical regions in the high dementia risk group compared to controls. In contrast, the low-risk group showed elevated neuroinflammation in only two cortical areas.

Interestingly, the study found that neuroinflammation was associated with worse cognitive performance, as measured by the Addenbrooke’s Cognitive Examination-III score. This correlation was particularly strong in the high dementia risk group, indicating that neuroinflammation could be a driving factor in the early cognitive decline seen in these patients.

In terms of tau accumulation, the findings were more nuanced. Increased 18F-AV-1451 binding in PD versus controls was primarily observed in subcortical regions known for off-target binding, with no significant relationship to cognitive decline. However, whole-brain tau burden did correlate with serum phosphorylated tau181 levels, suggesting that while regional tau accumulation might not be as prominent in early PD, it still plays a role in disease progression.

The study’s findings suggest that neuroinflammation could be an early, modifiable factor in the development of dementia in PD. This highlights the potential for immunomodulatory treatments to slow or prevent the onset of dementia in high-risk patients. Current anti-inflammatory treatments, already licensed for other conditions, could be repurposed for use in PD, offering a readily available therapeutic option.

Further research is needed to confirm these findings and explore the long-term benefits of targeting neuroinflammation in PD. Longitudinal follow-up of the NET-PDD cohort will be crucial in understanding how these early changes in brain inflammation and tau accumulation impact disease progression over time.

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