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Disease-specific tangle immunophenotypes distinguish hippocampal vulnerability in Alzheimer’s disease and Parkinson’s disease dementia
Schreiner S, Miranda de la Maza M, Hammer GP, Jeannelle F, Darricau M, Mirault D, Mechawar N, Netherlands Brain Bank et al.. bioRxiv, 2026-08-19
Topic: Plasma and spinal-fluid biomarkers
Structured Abstract INTRODUCTION Tau pathology typically occurs in Alzheimeŕs disease (AD), however is also frequently present in Parkinsońs disease dementia (PDD) and Dementia with Lewy Bodies (DLB), yet its disease-specific signature is unclear. METHODS Five tau, amyloid-β, α-synuclein and neuronal markers were analysed across hippocampal subfields in non-demented controls (CTLs), AD, PDD and DLB using multiplex immunohistochemistry, single-tangle classification and confocal imaging. RESULTS AT8, pTau217, and GT38 were predominatly detected in AD, while pS422 was enriched in PDD and pS396 showed a region- and disease-specific pattern. DLB resembled AD in subregional tau distribution. Tau marker correlation were different comparing AD, PDD and CTL. Single-tangle analyses revealed disease-specific immunophenotypes but conserved mature intra-tangle epitope organisation. Distinct tau signatures were associated with inhibitory interneuron vulnerability, while regional tau co-occurrence with amyloid-β and α-synuclein remained conserved. DISCUSSION Disease-specific tau signatures vary across hippocampal subregions and neuronal populations, implicating the contribution of regional and cell-specific factors beyond pathology burden.
Key findings
- RESULTS AT8, pTau217, and GT38 were predominatly detected in AD, while pS422 was enriched in PDD and pS396 showed a region- and disease-specific pattern.
- Single-tangle analyses revealed disease-specific immunophenotypes but conserved mature intra-tangle epitope organisation.
- Distinct tau signatures were associated with inhibitory interneuron vulnerability, while regional tau co-occurrence with amyloid-β and α-synuclein remained conserved.
Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 21 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 13 of the 62 points we could judge it on, which is 21 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (bioRxiv) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| 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 | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 13 / 62 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 13 of the 62 points we could judge it on is 21 out of 100. |
| Total | 21 / 100 | Capped to 16 because this is not a peer-reviewed article. |
What each of these 20 components measures, and what this score is not →
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APA 7th
Schreiner, S., Miranda de la Maza, M., Hammer, G. P., Jeannelle, F., Darricau, M., Mirault, D., et al. (2026). Disease-specific tangle immunophenotypes distinguish hippocampal vulnerability in Alzheimer’s disease and Parkinson’s disease dementia. bioRxiv. https://doi.org/10.64898/2026.08.13.744594
Vancouver
Schreiner S, Miranda de la Maza M, Hammer GP, Jeannelle F, Darricau M, Mirault D, et al. Disease-specific tangle immunophenotypes distinguish hippocampal vulnerability in Alzheimer’s disease and Parkinson’s disease dementia. bioRxiv. 2026. doi:10.64898/2026.08.13.744594.
BibTeX
@article{schreiner2026-ff9cb4d7,
author = {Schreiner, S. and Miranda de la Maza, M. and Hammer, G. P. and Jeannelle, F. and Darricau, M. and Mirault, D. and Mechawar, N. and Bank, Netherlands Brain and others},
title = {{Disease-specific tangle immunophenotypes distinguish hippocampal vulnerability in Alzheimer’s disease and Parkinson’s disease dementia}},
journal = {bioRxiv},
year = {2026},
doi = {10.64898/2026.08.13.744594},
url = {https://doi.org/10.64898/2026.08.13.744594}
}