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74/100

✓ Peer-reviewed alzhub usefulness score 74 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Results At randomization, the mean age is 72, 50% female, 77% with CDR-global score 0.5, and mean MMSE score 23.8. No significant differences between treatment groups were observed in the primary or secondary clinical endpoints. Significantly reduced CSF levels with neflamapimod treatment, relative to placebo, were evident for T-tau [difference (95% CI): -18.8 (-35.8, -1.8); P=0.031] and p-tau 181 [-2.0 (-3.6, -0.5); P=0.012], with a trend for neurogranin [-21.0 (-43.6, 1.6); P=0.068]. In pre-specified pharmacokinetic-pharmacodynamic (PK-PD) analyses, subjects in the highest quartile of trough plasma neflamapimod levels demonstrated positive trends, compared with placebo, in HLVT-R and WMS. Combined with PK-PD findings, the results indicate that a longer duration study of neflamapimod at a higher dose level to assess effects on AD progression is warranted.

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

APA 7th

Prins, N. D., Harrison, J. E., Chu, H. M., Blackburn, K., Alam, J. J., Scheltens, P., et al. (2021). A phase 2 double-blind placebo-controlled 24-week treatment clinical study of the p38 alpha kinase inhibitor neflamapimod in mild Alzheimer's disease. Alzheimer's research & therapy. https://doi.org/10.1186/s13195-021-00843-2

Vancouver

Prins ND, Harrison JE, Chu HM, Blackburn K, Alam JJ, Scheltens P, et al. A phase 2 double-blind placebo-controlled 24-week treatment clinical study of the p38 alpha kinase inhibitor neflamapimod in mild Alzheimer's disease. Alzheimer's research & therapy. 2021. doi:10.1186/s13195-021-00843-2. PMID: 34044875.

BibTeX

@article{prins2021-34044875,
  author  = {Prins, N. D. and Harrison, J. E. and Chu, H. M. and Blackburn, K. and Alam, J. J. and Scheltens, P. and {REVERSE-SD Study Investigators}},
  title   = {{A phase 2 double-blind placebo-controlled 24-week treatment clinical study of the p38 alpha kinase inhibitor neflamapimod in mild Alzheimer's disease}},
  journal = {Alzheimer's research \& therapy},
  year    = {2021},
  doi     = {10.1186/s13195-021-00843-2},
  pmid    = {34044875},
  url     = {https://doi.org/10.1186/s13195-021-00843-2}
}

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.

Key findings

Results At randomization, the mean age is 72, 50% female, 77% with CDR-global score 0.5, and mean MMSE score 23.8.
No significant differences between treatment groups were observed in the primary or secondary clinical endpoints.
Significantly reduced CSF levels with neflamapimod treatment, relative to placebo, were evident for T-tau [difference (95% CI): -18.8 (-35.8, -1.8); P=0.031] and p-tau 181 [-2.0 (-3.6, -0.5); P=0.012], with a trend for neurogranin [-21.0 (-43.6, 1.6); P=0.068].
In pre-specified pharmacokinetic-pharmacodynamic (PK-PD) analyses, subjects in the highest quartile of trough plasma neflamapimod levels demonstrated positive trends, compared with placebo, in HLVT-R and WMS.
Combined with PK-PD findings, the results indicate that a longer duration study of neflamapimod at a higher dose level to assess effects on AD progression is warranted.

Why it matters

In this 24-week phase 2 trial in mild Alzheimer's disease, the drug neflamapimod did not improve the main or secondary clinical measures compared with placebo. It did significantly lower spinal-fluid levels of total tau and p-tau 181, markers of nerve damage and tau disease. Combined with signals in people with the highest drug levels, the authors argue a longer, higher-dose study is warranted, so any clinical benefit remains unproven.

Study details

Study designclinical trial
Participants464
Effect sizeor 1.0
Evidence strengthHigh

How this study scored 74/100

Published in a peer-reviewed journal, and it is a randomised controlled trial.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Alzheimer's research & therapy)
Journal's citation record	1 / 4	Alzheimer s Research & Therapy: journal h-index 146 (OpenAlex, 2026-10-29)
Study design	11 / 12	A randomised controlled trial (from PubMed type “Randomized Controlled Trial”)
Strength of evidence	5 / 5	Rated “high” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	3 / 5	2021 — within 6 year(s) of the newest study here
Sample size	2 / 4	464 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)
Randomised / blinded	2 / 2	Randomised and blinded or placebo-controlled (as stated in the record)
Times cited	5 / 7	Cited 107 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	15.3 citations a year over 7 year(s) since 2021
Impact for its field and year	4 / 6	Cited 8.3× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 5 other studies in this library
Still being cited	3 / 4	Cited 66 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Philip Scheltens: h-index 181 (OpenAlex, whole career)
Institution's track record	1 / 3	King's College London: institution h-index 1,348 (OpenAlex)
Multi-centre collaboration	2 / 3	PubMed indexes it as a multicentre study
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 34044875)
Free to read	2 / 2	Free to read
Total	74 / 100	—

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