Abstract: Shared inflammatory programs in aging muscle and Alzheimer's brain tissue
In this abstract, aging skeletal muscle and Alzheimer's-related brain tissue showed convergent endothelial and myeloid inflammatory programs; related pathway-level signals appeared in blood, but gene-level blood associations did not survive correction. [1]
Automatic summary · not editorially reviewed
The key findings
The abstract reports transcriptomic analyses of skeletal muscle from 23 donors, a brain atlas from 84 donors and peripheral blood. [1]
Cross-tissue analysis found six concordantly enriched pathways with 109 genes in endothelial populations and four pathways with 51 genes in myeloid populations. [1]
In independent frailty and ADNI datasets, 23 of 30 pathway-subset tests were significantly enriched, but gene-level blood associations did not survive correction. [1]
The source at a glance
- Study type / format
- Abstract of a cross-tissue transcriptomic analysis with simulation-based regulator prioritization
- Population / context
- Human skeletal muscle donors (23), brain atlas donors (84, with 30 in an early score window) and peripheral-blood datasets including frailty and ADNI cohorts.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- October 8, 2026
Muscle, brain and blood datasets compared
The abstract describes analyses of independent, unpaired human transcriptomic datasets: skeletal muscle from 23 donors, the SEA-AD middle temporal gyrus atlas from 84 donors, and peripheral blood. Donor-aware models looked at age-associated changes in muscle and changes across a continuous pseudoprogression score in brain. Cross-tissue comparisons focused on 30 brain donors within an early score window.
Supporting source [1]
Convergent endothelial and myeloid programs reported
Aging muscle showed increased inflammatory, extracellular-matrix and stromal communication programs. During early Alzheimer's-related brain progression, vascular and immune populations showed increasing inflammatory and matrix-associated activity with shifts in intercellular communication. The cross-tissue analysis identified six concordantly enriched pathways with 109 leading-edge genes in endothelial populations and four pathways with 51 genes in myeloid populations. CellOracle simulations prioritized ETS2 and BHLHE40 as exploratory endothelial regulators.
Supporting source [1]
Blood signals mixed; hypotheses only
Related peripheral-blood signatures varied across cohorts and cell types. In independent frailty and ADNI mild cognitive impairment and Alzheimer's datasets, 23 of 30 predefined tissue-derived pathway-subset tests showed significant positive enrichment after false-discovery-rate correction, but individual gene-level bulk-blood associations did not survive correction. The authors call the cross-tissue programs and candidate regulators testable hypotheses. This is an abstract; the full text was not reviewed.
Supporting source [1]
How to interpret this
This explainer is based only on the abstract; the full text was not reviewed. The datasets were independent and unpaired, blood signatures varied across cohorts and cell types, and the proposed regulators and cross-tissue programs are described as testable hypotheses, not established mechanisms.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zhang A, Shen W, Yan S, Chen J, Liu X, Zou J, Li S, Hu S, Liu Y, Pan C, Lan Z, Peng G, Zhang Q, Peng W, Ahmadizar F, Zhang J, the Alzheimer’s Disease Neuroimaging Initiative. · europepmc.org · October 8, 2026