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Psychosis in Alzheimer Disease and Elevations in Disease-Relevant Biomarkers
Gomar JJ, Koppel J.. JAMA psychiatry, 2024-08-01
Topic: Amyloid, tau and blood-test diagnosis
Importance The emergence of psychotic symptoms in Alzheimer disease (AD) is associated with accelerated cognitive and functional decline that may be related to disease pathology. Results The cohort included 752 participants with AD (mean [SD] age, 74.2 [7.7] years; 434 male [57.7%]). In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01). The mean slope of p-tau181 change was significantly different in AD+P incident and AD+P baseline groups (F5,746 = 86.76, P Conclusions and relevance Results of this cohort study suggest that the emergence of psychosis in AD was associated with elevations in plasma levels of p-tau181, highlighting the potential utility of plasma p-tau181 as a biomarker of neuropsychiatric illness in AD, which could have implications for predictive and treatment response strategies.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gomar, J. J., & Koppel, J. (2024). Psychosis in Alzheimer Disease and Elevations in Disease-Relevant Biomarkers. JAMA psychiatry. https://doi.org/10.1001/jamapsychiatry.2024.1389
Vancouver
Gomar JJ, Koppel J. Psychosis in Alzheimer Disease and Elevations in Disease-Relevant Biomarkers. JAMA psychiatry. 2024. doi:10.1001/jamapsychiatry.2024.1389. PMID: 38922609.
BibTeX
@article{gomar2024-38922609,
author = {Gomar, J. J. and Koppel, J.},
title = {{Psychosis in Alzheimer Disease and Elevations in Disease-Relevant Biomarkers}},
journal = {JAMA psychiatry},
year = {2024},
doi = {10.1001/jamapsychiatry.2024.1389},
pmid = {38922609},
url = {https://doi.org/10.1001/jamapsychiatry.2024.1389}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Importance The emergence of psychotic symptoms in Alzheimer disease (AD) is associated with accelerated cognitive and functional decline that may be related to disease pathology.
- Results The cohort included 752 participants with AD (mean [SD] age, 74.2 [7.7] years; 434 male [57.7%]).
- In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01).
- The mean slope of p-tau181 change was significantly different in AD+P incident and AD+P baseline groups (F5,746 = 86.76, P < .0001) and when only individuals with amyloid-β positivity (Aβ+), which was determined using positron emission tomography, were compared (F5,455 = 84.60, P < .001).
Why it matters
In this cohort of 752 people with Alzheimer's disease, the new appearance of psychosis was linked to rising plasma p-tau181 levels. This points to plasma p-tau181 as a possible biomarker for neuropsychiatric symptoms, not as a treatment or cure.
New to this subject? Start with our plain-English guide: Blood tests & biomarkers →
Study details
- Study designcohort study
- Participants752
- Effect size57.7%; 52.4%
- Evidence strengthModerate
How this study scored 60/100
Published in a leading specialty journal, and it is a cohort study following people over time. Scored zero for randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (JAMA psychiatry) |
| Journal's citation record | 3 / 4 | JAMA Psychiatry: journal h-index 256 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A cohort study following people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2024 — within 3 year(s) of the newest study here |
| Sample size | 2 / 4 | 752 participants |
| Effect reported | 2 / 3 | Effect reported as a number, without an interval or test |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 17 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.2 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 3 / 6 | Cited 4.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 2 / 4 | Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jeremy L. Koppel: h-index 22 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Northwell Health: institution h-index 461 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 38922609) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 60 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1001/jamapsychiatry.2024.1389
- PubMed: 38922609
- Original source →
- Free full text: PubMed Central →
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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