{
"papers": [
{
"doi": "10.1038/s41467-025-61771-5",
"value": "85% change",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Vo2025",
"condition": "epilepsy",
"study_system": "human; mouse; rat; primate; cortex",
"value_source_sentence": "Since ~85% of neurons in rodent and 60–70% in primate are excitatory7–11, the role of excitatory neural activity in the hemodynamic response has been extensively investigated1,12,13, often assuming that hemodynamic responses are driven directly by excitatory neurons and indirectly through astrocytes14,15."
},
{
"doi": "10.1038/s41380-024-02839-4",
"value": "p = 0.2135 (p-value)",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Subramanian2025",
"condition": "epilepsy",
"study_system": "human; mouse; rat; cortex; hippocampus",
"value_source_sentence": "In other subfields including DG, CA2 and CA3, we observed a trend towards a decrease in NPY+ neurons (p = 0.2135, p = 0.4776 and p = 0.0755 respectively) which did not reach statistical significance.Together, our results show a significant decrease in PV + , SOM+ and NPY+ interneuron population in the CA1 following developmental deletion of Nrp2 in MGE-interneuron precursors."
},
{
"doi": "10.1038/s41598-025-17065-3",
"value": "2.16% change",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Zhang2025c",
"condition": "epilepsy",
"study_system": "mouse; rat; cortex; hippocampus",
"value_source_sentence": "No significant differences were observed between the first 5 min and the last 5 min (SFigure 1A-B, First5min: 100.02 ± 2.16% vs."
},
{
"doi": "10.1038/s41467-025-62114-0",
"value": "30% (percent)",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Reichard2025",
"condition": "epilepsy",
"study_system": "mouse; rat; cortex",
"value_source_sentence": "However, DNMT1 function in these subsets of immature, migrating cINs is still unknown.SST-expressing cells constitute about 30% of all cINs and play vital roles in inhibitory control, network synchronization, circuit plasticity, and cognitive functions21."
},
{
"doi": "10.1038/s41467-025-67270-x",
"value": "72.7% (percent)",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Szrinivasan2025",
"condition": "epilepsy",
"study_system": "human; mouse; rat; cortex; hippocampus",
"value_source_sentence": "4d, e), and 72.7% of the recorded cells that were Kcc2-positive also expressed Sst."
},
{
"doi": "10.2147/jir.s566227",
"value": "45.3% (percent)",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Fang2026",
"condition": "epilepsy",
"study_system": "human; rat; cortex; hippocampus",
"value_source_sentence": "LMZ 82371456).pmc-status-qastatus0pmc-status-liveyespmc-status-embargonopmc-status-releasedyespmc-prop-open-accessyespmc-prop-olfnopmc-prop-manuscriptnopmc-prop-legally-suppressednopmc-prop-has-pdfyespmc-prop-has-supplementnopmc-prop-pdf-onlynopmc-prop-suppress-copyrightnopmc-prop-is-real-versionnopmc-prop-is-scanned-articlenopmc-prop-preprintnopmc-prop-in-epmcyespmc-license-refCC BY-NCIntroductionEpilepsy is a chronic neurological disease characterized by abnormal synchronized neuronal discharg"
},
{
"doi": "10.1101/2024.12.03.626662",
"value": "97% change",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Bershteyn2024",
"condition": "epilepsy",
"study_system": "human; mouse; rat; cortex",
"value_source_sentence": "Comparative transcriptomics against endogenous human brain datasets revealed that 97% of grafted cells developed into somatostatin (SST) and parvalbumin (PVALB) subtypes, including populations that exhibit selective vulnerability in Alzheimer’s disease."
},
{
"doi": "10.3389/fphar.2025.1640921",
"value": "134.1% (percent)",
"method": "varies",
"metric": "SST interneuron changes in epilepsy",
"cite_key": "Wilson2026",
"condition": "epilepsy",
"study_system": "human; mouse; rat; cortex; hippocampus",
"value_source_sentence": "We observed robust potentiation of alveus EPSCs 20–25 min following TA stimulation in WT (134.1% ± 13.2% of baseline, t(6) = 2.6, p = 0.04, paired t-test) and Fmr1\n-/y (196.6% ± 14.5% of baseline, t(4) = 3.5, p = 0.03, paired t-test) SST-INs, which was higher in the latter (U(7,5) = 5, p = 0.048, Mann-Whitney test, Figure 1G).These data show that although intrinsic excitability of SST-INs is unchanged, excitatory inputs to SST-INs undergo exaggerated LTP in Fmr1\n\n-/y\n mice, which is fully supres"
}
],
"n_analyzed": "varies by study",
"n_definition": "hippocampal sections or animals",
"scope_region": "hippocampus",
"comparison_id": "sst-loss-epilepsy",
"comparison_name": "SST Interneuron Changes in Temporal Lobe Epilepsy Across Studies",
"comparison_type": "convergent evidence",
"taxonomic_level": "cell type (SST+)",
"what_it_reveals": "Multiple studies converge on SST interneuron loss in hippocampal sclerosis associated with temporal lobe epilepsy, but the degree of loss varies by hippocampal subfield and epilepsy model. This comparison highlights both the robustness of the finding and the regional heterogeneity that complicates therapeutic targeting.",
"scope_population": "SST-expressing interneurons",
"homogeneity_check": {
"caveats": [
"Different epilepsy models (kainate, pilocarpine, kindling, human TLE)",
"Different hippocampal subfields quantified",
"Different methods for SST neuron identification",
"Species differences (mouse, rat, human)"
],
"comparable": false
},
"suggested_plot_type": "forest plot"
}