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

John M Ringman1, James Luo2, Yonggand Shi3

  • 1Department of Neurology, Keck School of Medicine at USC, Los Angeles, CA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Autosomal dominant Alzheimer's disease (ADAD) mutations show distinct biomarker patterns. Amyloid PET imaging differences between PSEN1 and APP mutations vary by disease stage, offering insights into ADAD progression.

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Area of Science:

  • Neuroscience
  • Biomarker Research
  • Genetics

Background:

  • Autosomal dominant Alzheimer's disease (ADAD) presents neuropathological differences compared to late-onset AD.
  • Distinct variations exist among different ADAD mutations, necessitating specific investigations.
  • The PSEN1 (A431E) and APP (V717I) mutations are key genetic drivers of ADAD.

Purpose of the Study:

  • To compare fluid, MRI, PiB, and FDG PET biomarkers in carriers of A431E PSEN1 and V717I APP mutations.
  • To analyze biomarker differences at comparable clinical disease stages in ADAD.
  • To elucidate the impact of specific ADAD mutations on disease progression.

Main Methods:

  • Utilized data from the DIAN observational study (Data Freeze 15).
  • Categorized participants into asymptomatic (CDR=0), mildly symptomatic (CDR=0.5), and demented (CDR>0.5) groups.
  • Employed linear models to compare biomarkers (plasma Abeta42, FDG PET, PiB PET, MRI) between mutation carriers, adjusting for estimated years to symptom onset. PiB SUVRs were standardized to the corpus callosum; p<0.01 for significance.

Main Results:

  • Mildly symptomatic A431E PSEN1 carriers showed higher plasma Abeta42 than V717I APP carriers.
  • Asymptomatic V717I carriers exhibited reduced cerebral metabolism in specific brain regions compared to A431E carriers.
  • Amyloid PET (PiB SUVR) differences varied by mutation and disease stage, with notable regional variations in asymptomatic, mildly symptomatic, and demented carriers. No significant CSF or MRI volumetric differences were observed.

Conclusions:

  • Significant differences in amyloid PET imaging measures exist between A431E PSEN1 and V717I APP mutations.
  • These biomarker differences are stage-dependent, highlighting distinct pathological trajectories in ADAD.
  • Findings underscore the importance of considering specific mutation types in ADAD research and potential therapeutic strategies.