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The Interaction Between Neuroinflammation and β-Amyloid in Cognitive Decline in Parkinson's Disease. | LitMetric

The Interaction Between Neuroinflammation and β-Amyloid in Cognitive Decline in Parkinson's Disease.

Mol Neurobiol

Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada.

Published: January 2020

AI Article Synopsis

  • Activated microglia are linked to cognitive decline in Parkinson's disease (PD), particularly in patients with β-amyloid deposits, which are associated with faster cognitive deterioration.
  • The study examined 41 individuals: 17 with normal cognition, 12 with mild cognitive impairment, and 12 healthy controls, using specific radioligands to measure β-amyloid levels and microglial activation in various brain regions.
  • Findings revealed significant interactions between β-amyloid positivity and microglial activation in areas like the frontal lobe and striatum, suggesting a complex relationship that requires further investigation to determine whether amyloid deposits lead to neuroinflammation or if the microglial response is protective.

Article Abstract

Activated microglia have been reported to play an important role in Parkinson's disease (PD). A more rapid cognitive decline has been associated with deposits of β-amyloid. In this study, the aim was to evaluate the role of brain β-amyloid and its relationship with activated microglia in PD patients with normal and impaired cognition. We studied 17 PD patients with normal cognition (PDn), 12 PD patients with mild cognitive impairment (PD-MCI), and 12 healthy controls (HCs) with [C] Pittsburgh compound B (PIB) to assess the impact of β-amyloid deposition in the brain on microglial activation evaluated using the translocator protein 18-kDa (TSPO) radioligand [F]-FEPPA. [C] PIB distribution volume ratio was measured in cortical and subcortical regions. [F]-FEPPA total distribution volume values were compared for each brain region between groups to evaluate the effect of PIB positivity while adjusting for the TSPO rs6971 polymorphism. Factorial analysis of variance revealed a significant main effect of PIB positivity in the frontal lobe (F = 7.1, p = 0.012). Besides the frontal (p = 0.006) and temporal lobe (p = 0.001), the striatum (p = 0.018), the precuneus (p = 0.019), and the dorsolateral prefrontal cortex (p = 0.010) showed significant group × PIB positivity interaction effects. In these regions, PD-MCIs had significantly higher FEPPA V if PIB-positive. Our results indicate an interaction between amyloid-β deposition and microglial activation in PD. Further investigations are necessary to evaluate if amyloid deposits cause neuroinflammation and further neurodegeneration or if increased microglia activation develops as a protective response.

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Source
http://dx.doi.org/10.1007/s12035-019-01714-6DOI Listing

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