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Synapse Pathology in Schizophrenia: A Meta-analysis of Postsynaptic Elements in Postmortem Brain Studies
Amber Berdenis van Berlekom1,2, Cita H Muflihah2,3, Gijsje J L J Snijders1,2
1Department of Psychiatry, University Medical Center Utrecht Brain Center, Utrecht University, Utrecht, The Netherlands.
Schizophrenia Bulletin
|June 14, 2019
Summary
Schizophrenia (SCZ) is linked to reduced synapse density, particularly in cortical brain regions. This meta-analysis confirms a region-specific decrease in postsynaptic elements, offering a cellular hallmark for SCZ research.
Area of Science:
- Neuroscience
- Psychiatry
- Cell Biology
Background:
- Altered brain connectivity is a hallmark of schizophrenia (SCZ).
- Synapse density changes are implicated in SCZ pathology, but findings are heterogeneous.
- Previous studies have not clarified if synaptic changes are region-specific.
Purpose of the Study:
- To systematically review and quantitatively analyze literature on postsynaptic element density in SCZ.
- To determine if SCZ-related changes in synapse density are restricted to specific brain regions.
- To identify potential cellular hallmarks for understanding SCZ neuropathology.
Main Methods:
- Systematic literature review and random-effects meta-analysis of 31 postmortem studies.
- Included outcome measures: dendritic spine density (DSD), postsynaptic density (PSD) number, and PSD protein expression.
- Subgroup and exploratory analyses focused on cortical vs. subcortical tissues and specific brain regions.
Main Results:
- Overall decrease in postsynaptic element density in SCZ patients compared to controls (Hedges's g: -0.33, P = .020).
- Significant reduction observed in cortical tissues (Hedges's g: -0.44, P = .008) but not subcortical tissues.
- Dendritic spine density (DSD) showed a marked decrease (Hedges's g: -0.81, P = .004), particularly in the prefrontal cortex.
Conclusions:
- A region-specific decrease in postsynaptic element density is evident in schizophrenia.
- Cortical synaptic changes, especially DSD, represent a key cellular feature of SCZ.
- Findings provide a cellular basis for further research into SCZ brain dysconnectivity.
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