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Sam E Gandy1,2, Emilie L Castranio1, Merina Varghese1

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Summary
This summary is machine-generated.

Alzheimer's research shows non-fibrillar amyloid-beta oligomers (oAβ) impair learning and memory. This study reveals oAβ accumulation in Dutch mice causes synaptic and mitochondrial dysfunction, suggesting new diagnostic approaches.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) studies indicate cognitive decline does not correlate with fibrillar amyloid-beta (Aβ) burden.
  • Non-fibrillar Aβ species are increasingly implicated in AD pathogenesis.

Purpose of the Study:

  • To investigate the impact of Dutch mutant human amyloid precursor protein (hAPP) overexpression on cognitive function, synaptic plasticity, and mitochondrial health in a transgenic mouse model.
  • To characterize the accumulation and distribution of oligomeric Aβ (oAβ) in the brain and its correlation with behavioral deficits.

Main Methods:

  • Created transgenic mice overexpressing Dutch mutant hAPP (APPE693Q) under a pan-neuronal Thy1 promoter.
  • Utilized behavioral testing, immunohistochemistry (ICC), transmission electron microscopy (TEM), electrophysiology, and single-cell RNA sequencing.
  • Employed A11 and FITC-cyclic peptide (FITC-CP) fluorescence microscopy for oAβ detection and PET imaging with Lys(64Cu/NOTA)]-CP.

    • Main Results:

    • Dutch mice exhibited impaired learning behavior proportional to brain oAβ levels, with accumulation of non-fibrillar oAβ and alpha-CTFs but not Aβ fibrils.
    • Electrophysiological studies revealed abnormal presynaptic function, including impaired post-tetanic potentiation and synaptic fatigue.
    • Single-cell RNA-seq identified altered transcriptional profiles in excitatory neurons, associated with protein translation and oxidative phosphorylation defects, and reduced mitochondrial complex I activity.

    Conclusions:

    • Accumulation of Dutch oAβ is linked to age-related deficits in learning, presynaptic function, and mitochondrial structure and function.
    • Brain PET imaging using novel tracers may offer a method for monitoring oAβ levels and distribution in living subjects for AD diagnosis.