TRANSVERSE colon tissue in Alzheimer’s disease showed gut microbiome and proteome profile very closely tied to pathology in adults.
Alzheimer’s Disease Gut Microbiome Signals in Colon
Alzheimer’s disease has often been framed as a brain-first disorder, yet growing interest surrounds whether intestinal biology could relate to central nervous system pathology. In a new analysis of transverse colon tissue, investigators compared clinically and pathologically confirmed Alzheimer’s disease cases with control samples using combined proteomic profiling and microbial assessment. The goal was to characterize Alzheimer’s disease gut microbiome and protein patterns directly within colon tissue rather than relying only on stool-based signals.
Proteomic Patterns Suggest Immune and Metabolic Shifts
Across Alzheimer’s disease gut samples, pathways linked to antimicrobial humoral response and oxidative stress response were downregulated, while catabolic processes and insulin signaling were upregulated. Several proteins relevant to immune activity and synaptic biology differed between groups, including lower levels of complement components such as C5 and synaptic proteins such as synaptophysin. Amyloid beta 42 was detected at higher levels in the Alzheimer’s disease colon samples, reinforcing a tissue-level signal that may align with core Alzheimer’s pathology.
Tissue Microbial Differences Track With Clinical Burden
Microbial profiling also distinguished Alzheimer’s disease from controls. Amplicon sequence variants within Christensenellaceae, Desulfovibrio, and Candida tropicalis were higher in abundance in Alzheimer’s disease samples, while Streptococcus, Lachnospiraceae, Blautia, and Nakaseomyces were lower. Importantly, the overall bacterial composition correlated with Alzheimer’s disease clinical variables, including plaque and tangle burden, suggesting that intestinal community structure may reflect disease severity markers.
Clinical Takeaway
This study presents an in-depth view of the Alzheimer’s disease gut microbiome alongside proteomic changes in transverse colon tissue and highlights potential biomarker and therapeutic target directions. The findings do not establish causality, but they strengthen the rationale for continued work examining gut-linked mechanisms in Alzheimer’s disease pathogenesis.
Reference: Cheng Q et al. Gut proteome and microbiome alterations: Analysis of transverse colon samples from pathologically confirmed Alzheimer’s disease patients. Alzheimer’s Dement. 2026;22(1):e71021. doi: 10.1002/alz.71021.
