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Atypical Alzheimer's disease (AD) presentations stem from selective neuronal vulnerability to tau pathology, not comorbidities. Understanding these distinct tau-driven mechanisms is key to personalized AD treatments.

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Area of Science:

  • Neuroscience
  • Genomics
  • Pathology

Background:

  • Alzheimer's disease (AD) clinical heterogeneity is not fully explained by comorbid pathologies.
  • Recent evidence suggests selective neuronal vulnerability, particularly to tau, drives atypical AD phenotypes.
  • AD may result from a convergence of multiple pathogenic processes, not a single entity.

Purpose of the Study:

  • Clarify the basis of atypical AD manifestations.
  • Identify neuronal subpopulations vulnerable to tau pathology.
  • Delineate molecular pathways distinguishing typical from atypical AD.

Main Methods:

  • Postmortem brain samples from clinically characterized cases.
  • Classical neuropathology combined with single-nucleus RNA sequencing (snRNA-seq), transcriptomics, and proteomics.
  • Examination of subcortical sleep-wake regulation regions.

Main Results:

  • Comorbid neuropathologies did not significantly correlate with atypical AD presentations.
  • Specific neuronal populations, identified by snRNA-seq, show heightened tau pathology vulnerability in atypical AD.
  • Variant-specific tau burden in sleep-wake centers aligns with distinct sleep disturbances.

Conclusions:

  • Atypical AD variants reveal complex interplay between neuropathology and clinical outcomes.
  • Multi-omics integration captures AD's biological diversity, supporting a multi-process convergence model.
  • Findings guide personalized diagnostics, prognostics, and therapeutics for diverse AD presentations.