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

Babak Ahmadi1,2, Zohreh Morshedizad1,2, Hojjatollah Sadeqi1,2

  • 1University of Florida, Gainesville, FL, USA.

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

Co-occurring Alzheimer's disease (AD) and Lewy body (LB) pathology accelerate brain aging more than either condition alone. This highlights the need for combined biomarker assays and targeted treatments for these complex neurodegenerative conditions.

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Area of Science:

  • Neuroscience
  • Biomarkers
  • Neuroimaging

Background:

  • Alzheimer's disease (AD) and Lewy body (LB) pathology often coexist, but their combined impact on brain aging, atrophy, and function is not well understood.
  • Advances in α-synuclein seed amplification assays (SAA) allow for in vivo detection of LB pathology, providing new avenues to study its interaction with AD.

Purpose of the Study:

  • To investigate the synergistic effects of co-occurring AD and LB pathology on brain aging, atrophy, and cognitive function.
  • To utilize deep learning (DL) models and seed amplification assays (SAA) to quantify neurodegeneration in individuals with distinct AD and LB pathology profiles.

Main Methods:

  • A 3D-DenseNet deep learning model was trained on structural MRI data from 4,355 cognitively unimpaired individuals to estimate brain age.
  • In 803 cognitively impaired participants, α-synuclein positivity was determined by CSF SAA, and AD positivity by the p-tau181/Aβ42 ratio, classifying them into AD-LB-, AD-LB+, AD+LB-, and AD+LB+ subgroups.
  • Brain age gaps, region-specific atrophy, and cognitive performance were analyzed longitudinally across the four pathology subgroups.

Main Results:

  • The AD+LB+ subgroup exhibited the largest brain age gap, significantly exceeding that of single-pathology groups, indicating accelerated brain aging.
  • Sex-stratified analyses revealed sex-dependent vulnerabilities, with males showing higher brain age gaps in AD- subgroups and females in AD+ subgroups.
  • DL-driven saliency maps highlighted pronounced neurodegeneration in medial temporal, occipital, and basal ganglia regions for AD+LB+, correlating with accelerated atrophy and the most severe cognitive deficits.

Conclusions:

  • Co-occurring AD and LB pathology synergistically amplify neurodegeneration and accelerate brain aging.
  • The findings emphasize the critical importance of combined biomarker assays for diagnosing and managing individuals with co-existing AD and LB pathology.
  • Targeted interventions are crucial for addressing the amplified neurodegenerative effects observed in individuals with combined AD and LB pathology.