Predicted brain gene expression in OCD versus hoarding liability: senescence and apoptosis signals
In this abstract, genetically predicted brain expression linked to OCD liability showed apoptosis and complement signals, while hoarding-symptom liability showed a more senescence-like profile than OCD; the authors call these hypothesis-generating findings needing validation. [1]
Automatic summary · not editorially reviewed
The key findings
The study compared diagnosis-based OCD genetic liability with hoarding-symptom liability, not direct expression differences between diagnosed patient groups. [1]
Hoarding-symptom liability showed a more positive cellular-senescence profile than OCD (Mann-Whitney U p = 0.008861). [1]
The authors say the transcriptome-wide association findings require validation with colocalization, fine-mapping and functional studies. [1]
The source at a glance
- Study type / format
- Transcriptome-wide association study integrating GWAS summary statistics with brain eQTL reference panels (abstract).
- Population / context
- Genetic liability for OCD based on diagnosis and liability for hoarding symptoms, studied via summary statistics and brain expression reference panels.
- Summary based on
- Study abstract
- Original publication
- June 11, 2026
Liability-based comparison, not patient expression
The study compared genetic liability for OCD based on diagnosis with liability for hoarding symptoms, not direct expression differences between diagnosed patient groups. Large OCD and hoarding genome-wide association study summary statistics were combined with brain expression reference panels in a transcriptome-wide association approach. The resulting scores were read as genetically predicted expression associated with trait liability, not as measured tissue expression.
Supporting source [1]
Apoptosis and complement up, synapse pruning down in OCD
For OCD liability, the analysis reported positive enrichment for intrinsic apoptosis (Z = +5.707; permutation p = 0.005899) and for complement (Z = +4.932; p = 0.0164), plus a negative synapse-pruning profile (Z = -4.802; p = 0.0178). Hoarding-symptom liability showed a more positive cellular-senescence profile than OCD (Mann-Whitney U p = 0.008861; local false discovery rate 0.008861). Nicotinamide adenine dinucleotide (NAD)/sirtuin findings were directionally hoarding-skewed but exploratory.
Supporting source [1]
Hypothesis-generating signals across six brain regions
Gene-set enrichment was assessed across six brain regions using meta-analysis, permutation testing and paired phenotype comparisons. The authors describe the molecular signatures as divergent and hypothesis-generating: senescence/NAD-biased aging signals in hoarding, and apoptosis, complement-pruning and metabolic-reward dysregulation in OCD. They state that the transcriptome-wide association findings require validation with colocalization, fine-mapping and functional studies.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The scores are genetically predicted expression linked to trait liability, not measured tissue expression. Findings are described as hypothesis-generating and need colocalization, fine-mapping and functional validation; NAD/sirtuin results were exploratory.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.