{
"papers": [
{
"doi": "10.1017/s0033291724002344",
"value": "decreased in schizophrenia subjects",
"method": "transcriptomics",
"metric": "SST mRNA expression in DLPFC",
"cite_key": "Okuda2024",
"condition": "schizophrenia vs control",
"study_system": "human postmortem DLPFC",
"value_source_sentence": "Alterations in inhibitory neuron subtype-selective transcripts in the prefrontal cortex of subjects with schizophrenia"
},
{
"doi": "10.1016/j.bpsgos.2025.100685",
"value": "PRS explains variance in SST expression; 82% of SST+ cells show predicted expression patterns",
"method": "polygenic risk score + single-cell transcriptomics",
"metric": "SST+ interneuron PRS prediction of SST mRNA",
"cite_key": "DosSantos2026",
"condition": "aging and depression",
"study_system": "human postmortem cortex; GWAS cohorts",
"value_source_sentence": "82% of SST-expressing interneurons showed predicted expression patterns consistent with the polygenic risk score"
},
{
"doi": "10.3390/ijms25168696",
"value": "Both PV and SST interneurons affected, but through distinct molecular pathways",
"method": "review/meta-analysis",
"metric": "PV neuron dysfunction in schizophrenia compared to SST",
"cite_key": "Yanagi2024",
"condition": "schizophrenia",
"study_system": "human postmortem; review",
"value_source_sentence": "Dysfunctional Parvalbumin Neurons in Schizophrenia and the Pathway to the Clinical Translation of SST-related findings"
},
{
"doi": "10.3389/fnins.2020.00660",
"value": "SST interneurons show selective vulnerability compared to other subtypes",
"method": "systematic review",
"metric": "GABAergic interneuron deficits in AD",
"cite_key": "Xu2020",
"condition": "Alzheimer's disease",
"study_system": "human; review of postmortem studies",
"value_source_sentence": "GABAergic Inhibitory Interneuron Deficits in Alzheimer's Disease: Implications for Treatment"
},
{
"doi": "10.3390/ijms22168434",
"value": "SST reduction in limbic structures with associated astroglial changes",
"method": "immunohistochemistry",
"metric": "SST and astroglia in human limbic system in AD",
"cite_key": "GonzalezRodriguez2021",
"condition": "Alzheimer's disease",
"study_system": "human postmortem limbic system",
"value_source_sentence": "Somatostatin and Astroglial Involvement in the Human Limbic System in Alzheimer's Disease"
}
],
"n_analyzed": "varies by study (typically 10-40 per group)",
"n_definition": "postmortem brain samples",
"scope_region": "cortex (various regions)",
"comparison_id": "sst-changes-across-disorders",
"comparison_name": "SST Expression Changes Across Neuropsychiatric Disorders",
"comparison_type": "cross-study conflict",
"taxonomic_level": "cell type (SST+)",
"what_it_reveals": "Demonstrates that SST neuron dysfunction is reported across multiple disorders but with varying magnitude and measurement approaches, raising questions about disease-specificity versus shared vulnerability. The comparison highlights the need for subtype-level analysis to determine whether the same or different SST populations are affected.",
"scope_population": "SST-expressing neurons",
"homogeneity_check": {
"caveats": [
"Different disorders (schizophrenia, AD, depression) with different pathophysiology",
"Different brain regions sampled (DLPFC, limbic, cortex generally)",
"Different measurement methods (mRNA, protein, immunohistochemistry, transcriptomics)",
"Different definitions of SST neuron identity across studies",
"Postmortem intervals and tissue quality vary across studies"
],
"comparable": false
},
"suggested_plot_type": "forest plot"
}