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Basic Science and Pathogenesis.

Gowoon Son1, Mihovil Mladinov1, Felipe Luiz Pereira1

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Amnestic Alzheimer's disease (AD) shows greater degeneration in the suprachiasmatic nucleus (SCN) compared to atypical AD, impacting circadian rhythms. This highlights regional differences in AD-tau pathology and protein dysregulation.

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Area of Science:

  • Neuroscience
  • Pathology
  • Sleep Medicine

Background:

  • Alzheimer's disease (AD) variants exhibit distinct regional vulnerabilities to tau pathology.
  • Amnestic AD (amAD) shows blunted circadian rhythms compared to atypical AD (atypAD), with unknown neurobiological underpinnings.
  • Hypothesis: amAD involves greater degeneration of the suprachiasmatic nucleus (SCN) than atypAD.

Purpose of the Study:

  • Investigate neurobiological differences in the SCN between amAD and atypAD.
  • Examine the relationship between SCN degeneration, tau pathology, and circadian rhythm disturbances in AD variants.
  • Explore molecular dysfunctions contributing to differential AD susceptibility.

Main Methods:

  • Postmortem analysis of 27 SCN tissues (controls, amAD, atypAD).
  • Quantification of arginine vasopressin (AVP+) and vasoactive intestinal peptide (VIP+) neurons.
  • Semi-quantitative tau neurofibrillary counts and in-situ proteomics (GeoMx DSP) for 57 dysregulated proteins.

Main Results:

  • AtypAD had lower tau burden and higher SCN neuronal counts than amAD.
  • Differences were more pronounced in AVP+ neurons.
  • Spatial proteomics showed more preserved protein expression in atypAD compared to amAD.

Conclusions:

  • The SCN is more severely affected in amAD, with greater tau burden and neuronal loss, particularly in AVP+ neurons.
  • Regional vulnerability to AD-tau pathology contributes to AD variant phenotypes and blunted circadian rhythms in amAD.
  • Distinct molecular dysfunctions exist across AD variants, warranting further investigation into neuroinflammation and lysosomal pathways.