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Immune–proteo–metabolomic changes link to Aβ and tau pathology in Alzheimer disease
Meng Wang, Maria Buthut, Jenny Meinhardt, Carolin Otto, Gerardina Gallaccio, Camila Fernández‐Zapata, Matteo Teves, Claudia Samol et al.. Alzheimer s & Dementia, 2026-04-01
Topic: Amyloid, tau and blood-test diagnosis
Thirteen differentially expressed CSF proteins in A+T+ individuals correlated positively with tryptophan metabolites and pyroglutamate, and negatively with regulatory T cells, isobutyrate, and dendritic cells. Similar patterns were observed in blood. snRNA-seq suggested partial brain origin of metabolites. Our findings highlight conserved immune-metabolic-proteomic signatures in AD and implicate tryptophan metabolism as a cross-compartmental factor relevant for biomarker and therapeutic development. HIGHLIGHTS: Thirteen cerebrospinal fluid (CSF) proteins involved in metabolism and neuronal function link to Alzheimer's disease (AD) pathology Intergrative analysis reveals shared and compartment-specific AD signatures Tryptophan-kynurenine metabolites correlate with AD pathology Indole metabolites show CSF-plasma coupling in A+T+ individuals Immune signatures diverge across CSF (regulatory T cells [Tregs], dendritic cells [DCs]) and blood (B and myeloid cells).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wang, M., Buthut, M., Meinhardt, J., Otto, C., Gallaccio, G., Fernández‐Zapata, C., et al. (2026). Immune–proteo–metabolomic changes link to Aβ and tau pathology in Alzheimer disease. Alzheimer s & Dementia. https://doi.org/10.1002/alz.71359
Vancouver
Wang M, Buthut M, Meinhardt J, Otto C, Gallaccio G, Fernández‐Zapata C, et al. Immune–proteo–metabolomic changes link to Aβ and tau pathology in Alzheimer disease. Alzheimer s & Dementia. 2026. doi:10.1002/alz.71359. PMID: 41980911.
BibTeX
@article{wang2026-41980911,
author = {Wang, Meng and Buthut, Maria and Meinhardt, Jenny and Otto, Carolin and Gallaccio, Gerardina and Fernández‐Zapata, Camila and Teves, Matteo and Samol, Claudia and others},
title = {{Immune–proteo–metabolomic changes link to Aβ and tau pathology in Alzheimer disease}},
journal = {Alzheimer s \& Dementia},
year = {2026},
doi = {10.1002/alz.71359},
pmid = {41980911},
url = {https://doi.org/10.1002/alz.71359}
}
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Key findings
- Thirteen differentially expressed CSF proteins in A+T+ individuals correlated positively with tryptophan metabolites and pyroglutamate, and negatively with regulatory T cells, isobutyrate, and dendritic cells.
- Similar patterns were observed in blood. snRNA-seq suggested partial brain origin of metabolites.
- Our findings highlight conserved immune-metabolic-proteomic signatures in AD and implicate tryptophan metabolism as a cross-compartmental factor relevant for biomarker and therapeutic development.
- HIGHLIGHTS: Thirteen cerebrospinal fluid (CSF) proteins involved in metabolism and neuronal function link to Alzheimer's disease (AD) pathology Intergrative analysis reveals shared and compartment-specific AD signatures Tryptophan-kynurenine metabolites correlate with AD pathology Indole metabolites show CSF-plasma coupling in A+T+ individuals Immune signatures diverge across CSF (regulatory T cells [Tregs], dendritic cells [DCs]) and blood (B and myeloid cells).
Why it matters
In cerebrospinal fluid and blood samples, thirteen proteins linked to metabolism and neuronal function tracked with Alzheimer's pathology and with tryptophan metabolites. This is biomarker research and does not show that changing these pathways treats or prevents the disease.
Study details
- Participants19
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Alzheimer s & Dementia) |
| Journal's citation record | 2 / 4 | Alzheimer s & Dementia: journal h-index 228 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 1 / 4 | 19 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 3 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.5 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 4 / 6 | Cited 12.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Chotima Böttcher: h-index 31 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Charité - Universitätsmedizin Berlin: institution h-index 1,116 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41980911) |
| Free to read | 2 / 2 | Free to read |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
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