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Basic Science and Pathogenesis.

Giovanna Carello-Collar1, João Pedro Ferrari-Souza1, Marco Antônio De Bastiani1

  • 1Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

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|December 24, 2025
PubMed
Summary
This summary is machine-generated.

A specific reelin gene variant, RELN rs802787, appears to protect against Alzheimer's disease (AD) by reducing tau pathology, particularly in individuals with high amyloid-beta levels. This finding offers a potential new therapeutic target for late-onset AD.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • A rare reelin gene variant (RELN-COLBOS mutation) previously demonstrated resilience against Alzheimer's disease (AD) pathology.
  • The protective effect of common reelin gene single nucleotide polymorphisms (SNPs) against sporadic late-onset Alzheimer's disease (LOAD) remains uninvestigated.

Purpose of the Study:

  • To evaluate the impact of RELN SNPs on AD pathophysiology and cognitive decline in LOAD.
  • To determine if RELN variants confer resilience against amyloid-beta (Aβ) and tau accumulation.

Main Methods:

  • Analysis of 189 individuals from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort.
  • Assessment of RELN SNPs, Aβ and tau positron emission tomography (PET) imaging, cerebrospinal fluid (CSF) biomarkers, APOEε4 status, and cognitive tests (CDRSB, MMSE).
  • Linear regressions and mixed-effects models were used to investigate associations between RELN, Aβ, tau, and cognitive decline.

Main Results:

  • The RELN rs802787 SNP significantly protected against Aβ-driven tau pathology, particularly in the temporal lobe.
  • RELN rs802787 carriers showed reduced tau burden associated with APOEε4.
  • This protective effect on tau was observed in individuals with amyloid-beta but without tau pathology (A+T-), leading to slower cognitive decline.

Conclusions:

  • The RELN rs802787 variant confers resilience against Aβ-driven tau pathology and cognitive deterioration in LOAD.
  • Reelin signaling modulates tau accumulation and may reduce the impact of APOEε4 on tau burden.
  • RELN represents a promising therapeutic target for Alzheimer's disease.