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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, Bryan Rowe1, Claudia Alvarado1

  • 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.

The A431E mutation in PSEN1 causes more severe neurofibrillary tangle pathology, especially in the peri-Rolandic cortex. This may explain the spastic paraparesis seen in this Alzheimer's disease subtype.

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Area of Science:

  • Neuroscience
  • Genetics
  • Radiology

Background:

  • The PSEN1 A431E mutation, prevalent in Mexico, is linked to spastic paraparesis in Alzheimer's disease (AD).
  • The exact cause of spastic paraparesis in this AD subtype is not fully understood.
  • This study investigates neurofibrillary tangle deposition patterns in A431E mutation carriers.

Purpose of the Study:

  • To characterize neurofibrillary tangle (NFT) deposition in individuals with the PSEN1 A431E mutation.
  • To explore the relationship between NFT deposition and spastic paraparesis in this AD subtype.
  • To compare NFT patterns between A431E mutation carriers and other AD groups.

Main Methods:

  • Flortaucipir PET (FTP) scans and clinical evaluations were performed on 16 symptomatic A431E mutation carriers.
  • A comparison group included 20 individuals with non-spastic ADAD mutations or sporadic AD.
  • Standardized uptake value ratios (SUVRs) were calculated and compared between groups using t-tests.

Main Results:

  • A431E carriers showed significantly elevated FTP in widespread brain areas compared to controls.
  • NFT deposition was most pronounced in the para-, pre-, and post-central gyri in the A431E group.
  • Entorhinal cortex FTP SUVRs were non-significantly higher in the A431E cohort.

Conclusions:

  • The PSEN1 A431E mutation is associated with more severe neurofibrillary tangle pathology than other AD forms, even when matched for disease severity.
  • NFT deposition is particularly prominent in the peri-Rolandic cortex in A431E mutation carriers.
  • This enhanced pathology likely contributes to the spastic paraparesis observed in this specific AD subtype.