This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

39/100

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Inflammation and the immune system

Topic: Brain proteins, microglia and lab models

Plain-language summary

The findings demonstrate that administration of S1P analogs cP1P and P1P at 0.1 mg/kg and 1 mg/kg significantly reduced Aβ burden by inhibiting the amyloidogenic pathway and decreasing hyperphosphorylated tau protein levels in the mouse brain. Additionally, cP1P and P1P inhibited glial cell activation, as indicated by reduced GFAP and Iba-1 expression, and modulated neuroinflammatory markers, including p-NF-κB, TNF-α, and IL-1β. Furthermore, they regulated S1PR1-mediated Akt/mTOR signaling while preserving mitochondrial function by decreasing the expression levels of p-JNK, Caspase-3, and PARP-1. Moreover, the cP1P and P1P effectively restored synaptic markers such as PSD-95, SNAP-25, and Syntaxin, and significantly improved behavioral outcomes in the Aβ-treated mice. In vitro, results also demonstrated that the novel cP1P and P1P enhanced cell viability against Aβ toxicity.

What this study adds

Evidence grade: Low

In a mouse model, two sphingolipid compounds reduced amyloid burden and tau levels, calmed glial activation, and improved behavior. These are early animal findings, and it is not yet known whether they would work or be safe in people.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Choe, K., Ahmad, R., Kang, M. H., Lee, H. J., Ahmad, S., Park, T. J., et al. (2025). The novel sphingolipids cP1P and P1P attenuate neuroinflammation and enhance S1PR1/Akt/mTOR signaling to mitigate cognitive decline in an Alzheimer’s disease mouse model. Cell Communication and Signaling. https://doi.org/10.1186/s12964-025-02485-5

Vancouver

Choe K, Ahmad R, Kang MH, Lee HJ, Ahmad S, Park TJ, et al. The novel sphingolipids cP1P and P1P attenuate neuroinflammation and enhance S1PR1/Akt/mTOR signaling to mitigate cognitive decline in an Alzheimer’s disease mouse model. Cell Communication and Signaling. 2025. doi:10.1186/s12964-025-02485-5. PMID: 41204331.

BibTeX

@article{choe2025-41204331,
  author  = {Choe, Kyonghwan and Ahmad, Riaz and Kang, Min Hwa and Lee, Hyeon Jin and Ahmad, Sareer and Park, Tae Ju and Kim, Myeong Ok},
  title   = {{The novel sphingolipids cP1P and P1P attenuate neuroinflammation and enhance S1PR1/Akt/mTOR signaling to mitigate cognitive decline in an Alzheimer’s disease mouse model}},
  journal = {Cell Communication and Signaling},
  year    = {2025},
  doi     = {10.1186/s12964-025-02485-5},
  pmid    = {41204331},
  url     = {https://doi.org/10.1186/s12964-025-02485-5}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

The findings demonstrate that administration of S1P analogs cP1P and P1P at 0.1 mg/kg and 1 mg/kg significantly reduced Aβ burden by inhibiting the amyloidogenic pathway and decreasing hyperphosphorylated tau protein levels in the mouse brain.
Additionally, cP1P and P1P inhibited glial cell activation, as indicated by reduced GFAP and Iba-1 expression, and modulated neuroinflammatory markers, including p-NF-κB, TNF-α, and IL-1β.
Furthermore, they regulated S1PR1-mediated Akt/mTOR signaling while preserving mitochondrial function by decreasing the expression levels of p-JNK, Caspase-3, and PARP-1.
Moreover, the cP1P and P1P effectively restored synaptic markers such as PSD-95, SNAP-25, and Syntaxin, and significantly improved behavioral outcomes in the Aβ-treated mice.
In vitro, results also demonstrated that the novel cP1P and P1P enhanced cell viability against Aβ toxicity.

Why it matters

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 and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Cell Communication and Signaling)
Journal's citation record	1 / 4	Cell Communication and Signaling: journal h-index 133 (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	4 / 5	2025 — within 3 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	Laboratory or animal study (title names “mouse”) — scores zero
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	2 / 7	Cited 6 times (OpenAlex, 2026-10-10)
Citations per year	1 / 5	2.0 citations a year over 3 year(s) since 2025
Impact for its field and year	3 / 6	Cited 3.3× 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 6 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Myeong Ok Kim: h-index 67 (OpenAlex, whole career)
Institution's track record	1 / 3	Albert Einstein College of Medicine: institution h-index 973 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 3 institution(s) in 3 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 41204331)
Free to read	2 / 2	Free to read
Total	39 / 100	—

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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