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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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  11. Medial Temporal Lobe Atrophy Patterns In Early-versus Late-onset Amnestic Alzheimer's Disease

Medial temporal lobe atrophy patterns in early-versus late-onset amnestic Alzheimer's disease

Anika Wuestefeld1, Alexa Pichet Binette2, Danielle van Westen3,4

  • 1Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Klinikgatan 28, Room C1103b, Lund, SE-22242, Sweden. anika.wuestefeld@med.lu.se.

Alzheimer'S Research & Therapy
|September 16, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Early-onset Alzheimer's disease (EOAD) shows medial temporal lobe (MTL) atrophy, similar to late-onset AD (LOAD) in tau pathology. This study examined MTL subfields in amnestic EOAD patients.

Area of Science:

  • Neurology
  • Neuroimaging
  • Alzheimer's Disease Research

Background:

  • Medial temporal lobe (MTL) is thought to be spared in early-onset Alzheimer's disease (EOAD).
  • Detailed analysis of MTL subfields and atrophy drivers in amnestic EOAD is limited.
  • Understanding MTL involvement is crucial for diagnosing and treating Alzheimer's disease (AD).

Purpose of the Study:

  • To investigate medial temporal lobe (MTL) subfield atrophy in early-onset Alzheimer's disease (EOAD).
  • To compare atrophy patterns and co-pathologies between amnestic EOAD and late-onset AD (LOAD).
  • To identify drivers of atrophy in amnestic EOAD.

Main Methods:

  • Utilized data from the BioFINDER-2 study, including participants with memory impairment and abnormal amyloid-β and tau-PET scans.
Keywords:
AgingAmnestic ADAmygdala segmentation protocolAmyloid-beta

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  • Included 41 amnestic EOAD individuals (≤65 years) and 154 late-onset AD (LOAD, ≥70 years) patients, plus amyloid-β-negative controls.
  • Measured MTL subregions and biomarkers for (co-)pathologies.

    • Main Results:

    • Both AD groups exhibited smaller MTL subregions compared to controls.
    • Atrophy patterns showed differences: LOAD had thinner entorhinal cortices than aEOAD; aEOAD had thinner parietal regions than LOAD.
    • aEOAD presented with lower white matter hyperintensities than LOAD; no differences in MTL tau-PET or TDP-43 positivity were observed.

    Conclusions:

    • Evidence supports MTL atrophy in amnestic EOAD.
    • MTL tau pathology and co-pathologies were similar between amnestic EOAD and LOAD.
    • Findings suggest distinct atrophy patterns but shared underlying pathologies in EOAD and LOAD.
    Early-onset
    In vivo
    Late-onset
    MRI
    Medial temporal lobe subregions
    TPD-43
    Tau-PET imaging