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Basic Science and Pathogenesis.

Tatiana Georgiades1, Eileen A Chandra1, Bshaier Allehyany2

  • 1Imperial College London, London, London, United Kingdom.

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Alzheimer's disease (AD) involves synapse loss, impacting cognition. This study reveals synaptic proteome changes in early AD, identifying potential targets for early therapeutic interventions.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genomics

Background:

  • Synapse loss is a key factor in Alzheimer's disease (AD) cognitive decline.
  • Previous studies indicated altered synaptic pathways and gene expression in AD brain tissue.
  • The local synaptic transcriptome is crucial for synaptic plasticity and cognitive function.

Purpose of the Study:

  • To characterize molecular changes in mid-stage Alzheimer's disease (AD) by integrating proteomic and transcriptomic data from isolated synaptoneurosomes.
  • To investigate the role of local protein synthesis in synaptic protein expression in AD.
  • To identify potential targets for early therapeutic interventions in AD.

Main Methods:

  • Utilized post-mortem human middle temporal gyrus tissue from 33 AD cases (Braak III-IV) and 33 non-diseased controls (NDC, Braak 0-II).
  • Isolated synaptoneurosomes using the SynPER method.
  • Performed label-free quantitative proteomics (LC-MS/MS) and bulk RNA-seq, integrating data with Omix v1.0.0.
  • Conducted histopathological characterization for β-Amyloid and pTau (PHF1).

Main Results:

  • Downregulated mitochondrial function observed in mid-stage AD synaptoneurosomes.
  • Increased involvement of the pre-synaptic active zone in AD compared to controls, without significant pre- vs. post-synaptic compartment differences.
  • Differential expression analysis revealed the role of local protein synthesis in synaptic protein expression.
  • Multi-Omics Factor Analysis determined the contribution of amyloid and tau pathology to observed variations.

Conclusions:

  • Elucidated changes in the synaptic proteome preceding widespread synapse loss in AD.
  • Identified potential underlying mechanisms contributing to synaptic alterations in AD.
  • Provided insights into potential targets for early therapeutic interventions in Alzheimer's disease.