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Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex.

Katalin Völgyi1, Péter Gulyássy2, Mihail Ivilinov Todorov3,4

  • 1MTA-ELTE NAP B Laboratory of Molecular and Systems Neurobiology, Institute of Biology, Hungarian Academy of Sciences and Eötvös Loránd University, Pázmány Péter sétány 1C, Budapest, H-1117, Hungary. katvolgyi@gmail.com.

Molecular Neurobiology
|June 17, 2017
PubMed
Summary

Chronic cerebral hypoperfusion (CCH) alters synaptic proteins in the rat brain, impacting metabolism and neurotransmission. These synaptic changes may precede dementia, highlighting their role in vascular dementia development.

Keywords:
Alzheimer’s diseaseApolipoprotein EChronic cerebral hypoperfusionGABAergic synapseLabel-free LC-MS/MSSynaptic proteomeVascular dementia

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Area of Science:

  • Neuroscience
  • Proteomics
  • Vascular Biology

Background:

  • Chronic cerebral hypoperfusion (CCH) is linked to mild cognitive impairment (MCI), vascular dementia, and Alzheimer's disease (AD).
  • The mechanisms by which CCH induces neurodegeneration and its synaptic proteome-level changes in the cerebral cortex are not fully understood.

Purpose of the Study:

  • To investigate synaptic protein alterations in the cerebral cortex following CCH induced by bilateral common carotid artery occlusion (BCCAO) in a rat model.
  • To determine if these synaptic changes precede the onset of dementia-like symptoms.

Main Methods:

  • Rats underwent stepwise BCCAO to induce CCH, with occlusion confirmed via magnetic resonance angiography.
  • Synaptosome fractions were isolated from the cerebral cortex 7 weeks post-occlusion.
  • Label-free nanoUHPLC-MS/MS was used to analyze synaptic protein differences between CCH and sham-operated groups.

Main Results:

  • 46 proteins showed altered abundance in CCH rats.
  • Increased levels of synaptic protein/lipid metabolism and GABA shunt-related proteins were observed.
  • Decreased levels of neurotransmission and synaptic assembly-related proteins were identified.
  • Elevated synaptic apolipoprotein E (APOE) levels were implicated through network analysis and confirmed by Western blotting.

Conclusions:

  • CCH induces significant synaptic protein changes in the cerebral cortex.
  • Altered synaptic proteins, particularly APOE, may play a crucial role in the early stages of vascular dementia.
  • These synaptic proteome changes precede dementia-like symptoms, offering potential biomarkers for early detection.