ArticleInternational journal of molecular sciences2026
Batch- and Composition-Controlled Reanalysis of Bulk and Single-Nucleus Transcriptomes Reveals Co-Enrichment of Glial Complement and of Translational Signatures in Parkinson's Disease and Amyotrophic Lateral Sclerosis.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Failure of axonal maintenance is proposed as a mechanism shared by Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). We reanalysed three public post-mortem resources under one rule set: bulk RNA-seq of 1242 samples from 319 donors (GSE153960) and midbrain single-nucleus RNA-seq (GSE157783, GSE178265). As a contributing project, a second batch variable tracked diagnosis in both cord segments and was completely separated from it in three cortical regions, which we removed. Adjusting for this removed a third of the naive differential expression. In ALS cord, the dominant depleted program was microtubule-based axonal transport (normalised enrichment score -2.40, FDR < 0.001); a regeneration-associated panel reached significance in none of ten fits. An ALS cord signature carried into the PD midbrain and scored highest on microglia in all 11 donors (+3.55 versus +0.73 next). Of 86 gene sets significant in both diseases, a translation block contained the GCN2 amino-acid-deficiency response. Both axes are compartment-level: within PD microglia, the complement panel is null (+0.21,
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