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Related Concept Videos

Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

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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.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
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Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

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Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
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Updated: Jan 7, 2026

Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Juan Antonio Kim Hoo Chong Chie1, Scott A Persohn2, Adrian L Oblak2

  • 1Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

The phospholipase C gamma 2 (PLCG2) gene variant exacerbates Alzheimer's disease risk, but its interaction with a high-fat diet (HFD) may regulate disease progression. This study investigates PLCG2's role in Alzheimer's disease (AD) pathogenesis.

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Area of Science:

  • Neuroscience
  • Genetics
  • Metabolic Disorders

Background:

  • MODEL-AD has developed novel mouse models to better mimic human late-onset Alzheimer's disease (LOAD) for preclinical research.
  • Over 40 LOAD risk factor models have been created and assessed for relevance.
  • This study focuses on understanding how variations in the phospholipase C gamma 2 (PLCG2) gene influence LOAD risk, with or without a high-fat diet (HFD).

Purpose of the Study:

  • To determine the mechanisms by which PLCG2 variations drive increased risk for LOAD.
  • To investigate the combined effects of PLCG2 variants and HFD on LOAD pathogenesis.
  • To elucidate the role of PLCG2 in neuroinflammation and brain metabolism in the context of LOAD.

Main Methods:

  • Generated mice with the M28L variant in PLCG2 (PLCG2*M28L) on a LOAD2 background (B6.APOE4.Trem2*R47H.hAβ) using CRISPR/CAS9.
  • Administered control or HFD to LOAD2 and LOAD2.Plcg2*M28L mice to induce neuroinflammation.
  • Performed transcriptional profiling, uncoupling analysis, connectomics, and in vivo brain perfusion/glycolytic metabolism assessment (PET/CT) at 18 months.

Main Results:

  • Both HFD and PLCG2*M28L induced prodromal phenotypes (increased 18F-FDG uptake, increased cerebral blood flow).
  • The combination of PLCG2*M28L and HFD resulted in a Type 2 uncoupling phenotype (increased 18F-FDG uptake, decreased cerebral blood flow), indicating non-additive effects.
  • Connectomics revealed sex-specific differences in brain network organization, with PLCG2*M28L on HFD showing fewer clusters and altered network properties.

Conclusions:

  • PLCG2 variants and HFD similarly impact brain end-biology, suggesting PLCG2 is involved in inflammatory processes akin to HFD.
  • PLCG2 appears to modulate the inflammatory response to HFD in a regulatory manner, potentially reducing disease severity.
  • The study highlights the complex interplay between genetic risk factors and dietary components in LOAD pathogenesis.