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Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease
Ma QL, Teng E, Zuo X, Jones M, Teter B, Zhao EY, Zhu C, Bilousova T et al.. Neurobiology of disease, 2018-03-06
Topic: Brain proteins, microglia and lab models
Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). Apolipoprotein ε4 (APOE4) is the most common genetic risk factor for both familial AD (FAD) and sporadic AD; it accelerates Aβ aggregation and selectively impairs glutamate receptor function and synaptic plasticity. However, its molecular mechanisms remain elusive and these synaptic deficits are difficult to monitor. AD- and APOE4-dependent plasma biomarkers have been proposed, but synapse-related plasma biomarkers are lacking. We evaluated neuronal pentraxin 1 (NP1), a potential CNS-derived plasma biomarker of excitatory synaptic pathology. NP1 is preferentially expressed in brain and involved in glutamate receptor internalization. NP1 is secreted presynaptically induced by Aβ oligomers, and implicated in excitatory synaptic and mitochondrial deficits. Levels of NP1 and its fragments were increased in a correlated fashion in both brain and plasma of 7-8 month-old E4FAD mice relative to E3FAD mice. NP1 was also found in exosome preparations and reduced by dietary DHA supplementation. Plasma NP1 was higher in E4FAD+ (APOE4 +/+ /FAD +/- ) relative to E4FAD- (non-carrier; APOE4 +/+ /FAD -/- ) mice, suggesting NP1 is modulated by Aβ expression. Finally, relative to normal elderly, plasma NP1 was also elevated in patients with mild cognitive impairment (MCI) and elevated further in the subset who progressed to early-stage AD. In those patients, there was a trend towards increased NP1 levels in APOE4 carriers relative to non-carriers. These findings indicate that NP1 may represent a potential synapse-derived plasma biomarker relevant to early alterations in excitatory synapses in MCI and early-stage AD.
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APA 7th
Ma, Q. L., Teng, E., Zuo, X., Jones, M., Teter, B., Zhao, E. Y., et al. (2018). Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2018.02.014
Vancouver
Ma QL, Teng E, Zuo X, Jones M, Teter B, Zhao EY, et al. Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease. Neurobiology of disease. 2018. doi:10.1016/j.nbd.2018.02.014. PMID: 29501530.
BibTeX
@article{ma2018-29501530,
author = {Ma, Q. L. and Teng, E. and Zuo, X. and Jones, M. and Teter, B. and Zhao, E. Y. and Zhu, C. and Bilousova, T. and others},
title = {{Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease}},
journal = {Neurobiology of disease},
year = {2018},
doi = {10.1016/j.nbd.2018.02.014},
pmid = {29501530},
url = {https://doi.org/10.1016/j.nbd.2018.02.014}
}
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Key findings
- These findings indicate that NP1 may represent a potential synapse-derived plasma biomarker relevant to early alterations in excitatory synapses in MCI and early-stage AD.
Why it matters
In mice and in people, plasma levels of neuronal pentraxin 1 were elevated in early Alzheimer's disease and mild cognitive impairment, and in mice the protein was reduced by dietary DHA supplementation. The authors propose NP1 as a possible synapse-related blood biomarker, but this is early research and does not establish any treatment.
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Study details
- Evidence strengthLow
How this study scored 39/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of disease) |
| Journal's citation record | 2 / 4 | Neurobiology of Disease: journal h-index 225 (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 | 2 / 5 | 2018 — within 10 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 | 3 / 7 | Cited 32 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.2 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 2 / 6 | Cited 3.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 1 / 4 | Cited 7 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Gregory M. Cole: h-index 37 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Johns Hopkins University: institution h-index 2,306 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 8 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29501530) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 39 / 100 | — |
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