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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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Related Experiment Video

Updated: Jan 7, 2026

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

Stephanie A Schultz1, Lei Liu2, Hyun-Sik Yang3,4

  • 1Massachusetts General Hospital, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

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

Autosomal dominant Alzheimer's disease progression is driven by specific genetic mutations affecting gamma-secretase function and amyloid-beta production. Understanding these variant-level effects offers new therapeutic targets for Alzheimer's disease.

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Area of Science:

  • Genetics
  • Neuroscience
  • Biochemistry

Background:

  • Autosomal dominant Alzheimer's disease (ADAD) offers insights into Alzheimer's disease (AD) pathobiology.
  • Pathogenic variants in PSEN1 or PSEN2 are primary causes of ADAD, influencing gamma-secretase activity and amyloid-beta (Aβ) peptide production.
  • Significant heterogeneity in ADAD symptom onset necessitates examining variant-specific impacts on disease progression.

Purpose of the Study:

  • To investigate whether variant-level differences in gamma-secretase function and Aβ production explain the heterogeneity in ADAD progression.
  • To correlate in vitro measured Aβ production profiles with clinical, cognitive, and biomarker data in individuals with ADAD.

Main Methods:

  • Assessed Aβ peptide production from 161 PSEN1 and 70 PSEN2 pathogenic variants in vitro.
  • Utilized clinical, cognitive, and biomarker data from the Dominantly Inherited Alzheimer's Network Observational Study (DIAN).
  • Correlated in vitro Aβ production with age of symptom onset (AAO) and in vivo disease progression measures.

Main Results:

  • PSEN1 variant Aβ production strongly correlated with AAO, with more aberrant gamma-secretase function linked to earlier onset.
  • PSEN2 variant Aβ production showed associations with AAO, varying based on homology with PSEN1.
  • In vitro Aβ production profiles predicted clinical, cognitive, and biomarker trajectories in ADAD, improving upon AAO estimates.

Conclusions:

  • Variant-specific effects on gamma-secretase function and Aβ production fundamentally shape ADAD progression.
  • Findings provide strong support for the amyloid hypothesis of AD.
  • Gamma-secretase modulation (GSM) emerges as a promising therapeutic strategy for AD.