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Clinical Manifestations.

Jia Dong James Wang1, Yi Jin Leow2, Ashwati Vipin3

  • 1Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore, Singapore.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
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Summary
This summary is machine-generated.

This study identifies distinct biomarkers for hypoperfusion and neuroinflammation in mild cognitive impairment (MCI). Understanding these differences is key for developing targeted treatments for cognitive decline.

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Area of Science:

  • Neuroscience
  • Biomarkers
  • Cognitive Health

Background:

  • Mild cognitive impairment (MCI) involves interrelated processes of cerebral hypoperfusion and neuroinflammation.
  • These processes can create a cycle of oxidative stress and inflammation, contributing to cognitive decline.
  • Distinct cognitive and plasma biomarker profiles may differentiate vascular and inflammatory causes of MCI.

Purpose of the Study:

  • To investigate distinct cognitive and plasma biomarker profiles in a Southeast Asian cohort.
  • To differentiate between vascular (hypoperfusion-predominant) and inflammatory-driven cognitive impairments in MCI.
  • To explore the interplay between hypoperfusion and neuroinflammation in MCI.

Main Methods:

  • Participants with MCI were classified into hypoperfusion-predominant (P+), neuroinflammation-predominant (I+), and control (p-) groups using MRI and Glial Fibrillary Acidic Protein (GFAP) levels.
  • Cognitive performance and plasma biomarker profiles were compared across the three groups.
  • Mediation analysis was used to examine interactions between hypoperfusion and neuroinflammation.

Main Results:

  • The P+ group showed elevated Neurofilament Light Chain (NfL) levels.
  • The I+ group exhibited higher NfL, elevated Oligomeric Amyloid-Beta (OAB), a reduced Amyloid-Beta 42/40 (Aβ42/40) ratio, and lower global cognitive performance (VCAT) compared to the P+ group.
  • Neuroinflammation mediated the link between hypoperfusion and NfL, while reduced perfusion mediated neuroinflammation's effect on cognitive decline.

Conclusions:

  • Distinct biomarkers can differentiate neuroinflammation-predominant and hypoperfusion-predominant MCI.
  • Hypoperfusion and neuroinflammation have an interdependent relationship contributing to MCI.
  • Personalized therapies are needed to address both cerebrovascular and inflammatory factors in MCI, considering regional variations.