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Temporal lobe proteins implicated in synaptic failure exhibit differential expression and deamidation in vascular
Xavier Gallart-Palau1, Aida Serra1, Jingru Qian1
1School of Biological Sciences, Nanyang Technological University, Singapore.
Neurochemistry International
|December 16, 2014
Summary
Researchers identified key protein changes in vascular dementia (VaD) brains, revealing synaptic protein alterations and modifications that may drive cognitive decline. These findings highlight potential targets for treating synaptic failure in VaD.
Area of Science:
- Neuroscience
- Proteomics
- Biochemistry
Background:
- Synaptic failure is an early event in neurodegenerative disorders, preceding neuronal loss and cognitive decline.
- The specific proteins and posttranslational modifications causing synaptic failure in vascular dementia (VaD) are not well understood.
Purpose of the Study:
- To investigate the synapse-associated proteome in post-mortem human cortex from VaD patients and age-matched controls.
- To identify specific proteins and posttranslational modifications involved in synaptic failure in VaD.
Main Methods:
- Utilized isobaric tag for relative and absolute proteomic quantitation (iTRAQ) for proteomic profiling.
- Analyzed synapse-associated proteins in brain tissue from VaD patients and controls.
Main Results:
- Significant down-regulation of synaptic proteins, including clathrin and GDI1, was observed in VaD.
- Up-regulation of proteins such as SNAP25, bassoon, excitatory amino acid transporter 2, and Ca(2+)/calmodulin dependent kinase II in VaD.
- Identified a specific deamidation of synapsin1 in VaD, potentially affecting protein structure.
Conclusions:
- The study reveals altered protein expression and modification patterns in the synaptic proteome of VaD patients.
- These findings suggest potential molecular targets for therapeutic interventions aimed at preventing synaptic failure and cognitive decline in VaD.
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