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Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
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Biomarkers.

Liangyu Huang1

  • 1Qingdao Municipal Hospital, Qingdao, Shandong, China.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary

Progranulin (PGRN) and soluble triggering receptor expressed on myeloid cells-2 (sTREM2) levels in cerebrospinal fluid are linked to Alzheimer's disease (AD) pathology. Their interplay influences amyloid-beta (Aβ) metabolism, suggesting roles in lysosome function and neuroinflammation.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Progranulin (PGRN) and soluble triggering receptor expressed on myeloid cells-2 (sTREM2) are emerging biomarkers in Alzheimer's disease (AD).
  • Their specific roles and interactions in AD pathophysiology, particularly concerning amyloid-beta (Aβ) pathology, require further elucidation.

Purpose of the Study:

  • To investigate the associations of cerebrospinal fluid (CSF) PGRN and sTREM2 with AD biomarkers.
  • To explore the interplay between PGRN and sTREM2 in modulating Aβ pathology across the AD spectrum.

Main Methods:

  • Analysis of cross-sectional data from the CABLE (n=905) and ADNI (n=973) cohorts, classified using the A/T/N biomarker framework.
  • Statistical analyses including ANCOVA, post hoc comparisons, multiple linear regression, and bidirectional causal mediation analyses.

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Main Results:

  • CSF PGRN and sTREM2 levels showed distinct patterns across different A/T/N biomarker profiles.
  • Significant positive association between CSF PGRN and sTREM2 was observed across various A/T/N profiles.
  • Bidirectional mediation roles of PGRN and sTREM2 in modulating Aβ pathology were confirmed in both cohorts.

Conclusions:

  • The findings suggest a significant interplay between PGRN and sTREM2 in the context of Alzheimer's disease.
  • This interaction may play a crucial role in regulating amyloid metabolism through mechanisms involving lysosome function and microglia-related neuroinflammation.