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Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

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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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Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
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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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Dried Blood Spot Collection of Health Biomarkers to Maximize Participation in Population Studies
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Biomarkers.

Marcel Seungsu Woo1, Joseph Therriault2, Yi-Ting Wang2

  • 1University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 26, 2025
PubMed
Summary
This summary is machine-generated.

Neuroinflammation and cell death pathways drive Alzheimer's disease (AD) progression, even in preclinical stages. Early intervention targeting these processes is crucial for managing AD.

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Neuroinflammation is a key feature of Alzheimer's disease (AD), contributing to amyloid-beta (Aβ) and neurofibrillary tangle (NFT) accumulation.
  • The specific role of neuroinflammation in the progression of preclinical AD remains unclear.

Purpose of the Study:

  • To investigate the role of neuroinflammation in the progression of Alzheimer's disease (AD) across different cognitive stages.
  • To identify specific biological pathways associated with neuroinflammation and AD progression.

Main Methods:

  • Utilized Nucleic acid Linked Immuno-Sandwich Assay (NULISA) for targeted proteomics in diverse participant groups, including cognitively unimpaired individuals, those with mild cognitive impairment, AD patients, and controls.
  • Employed unsupervised analyses, cross-sectional associations, and longitudinal follow-up (mean 26 months) with PET imaging (Aβ, tau), MRI, and blood phospho-tau (p-tau) analytes.

Main Results:

  • CSF signatures for glia activation, immune signaling, and calcium signaling increased with aging and across the AD continuum, appearing early in cognitively unimpaired individuals with amyloid positivity (CU A+).
  • Longitudinal data in CU participants showed increased neuroinflammation, glia activation, cell death pathways, and mitochondrial transport deficits specifically in A+ individuals, correlating with p-tau217 progression.
  • Mediation analyses indicated that cell death pathways and glia activation mediate the effect of early AD progression (p-tau217) on neuroinflammation, with synaptic signaling and mitochondrial transport influencing cell death pathway activation.

Conclusions:

  • Neuroinflammation and cell death pathways are significant drivers of disease progression in preclinical and early AD.
  • Aβ may trigger a cycle of neuroinflammation, glia activation, and neuronal dysfunction, highlighting the need for early immunomodulatory interventions in AD.