Evidence map›Paper›PMID 28482641›Full record

Trial reportJournal of Alzheimer's disease : JAD2017

Bryostatin Effects on Cognitive Function and PKCɛ in Alzheimer's Disease Phase IIa and Expanded Access Trials.

Thomas J Nelson, Miao-Kun Sun, Chol Lim, Abhik Sen, Tapan Khan, Florin V Chirila, Daniel L Alkon

Open access · bronzeAbstract readClinical Trial, Phase IIRandomized Controlled Trial
In one paragraph

Trial report in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Vascular cognitive impairment and dementia: Prevention, treatments, mechanisms and management options for the future.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  8. Review
  9. Article
  10. Review
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  14. Article
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  16. Review
  17. Review
  18. Marine-derived Compounds: A Powerful Platform for the Treatment of Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024
    Review
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Thomas J NelsonBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Miao-Kun SunBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Chol LimBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Abhik SenBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Tapan KhanBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Florin V ChirilaBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Daniel L AlkonBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
West Virginia University · USBlanchette Rockefeller Neurosciences Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bryostatin 1, a potent activator of protein kinase C epsilon (PKCɛ), has been shown to reverse synaptic loss and facilitate synaptic maturation in animal models of Alzheimer's disease (AD), Fragile X, stroke, and other neurological disorders. In a single-dose (25 μg/m2) randomized double-blind Phase IIa clinical trial, bryostatin levels reached a maximum at 1-2 h after the start of infusion. In close parallel with peak blood levels of bryostatin, an increase of PBMC PKCɛ was measured (p = 0.0185) within 1 h from the onset of infusion. Of 9 patients with a clinical diagnosis of AD, of which 6 received drug and 3 received vehicle within a double-blind protocol, bryostatin increased the Mini-Mental State Examination (MMSE) score by +1.83±0.70 unit at 3 h versus -1.00±1.53 unit for placebo. Bryostatin was well tolerated in these AD patients and no drug-related adverse events were reported. The 25 μg/m2 administered dose was based on prior clinical experience with three Expanded Access advanced AD patients treated with bryostatin, in which return of major functions such as swallowing, vocalization, and word recognition were noted. In one Expanded Access patient trial, elevated PKCɛ levels closely tracked cognitive benefits in the first 24 weeks as measured by MMSE and ADCS-ADL psychometrics. Pre-clinical mouse studies showed effective activation of PKCɛ and increased levels of BDNF and PSD-95. Together, these Phase IIa, Expanded Access, and pre-clinical results provide initial encouragement for bryostatin 1 as a potential treatment for AD.

Indexed as

Alzheimer DiseaseCognition DisordersAdultAgedAged, 80 and overAnalysis of VarianceAnimalsAntipsychotic AgentsBrainBrain-Derived Neurotrophic FactorBryostatinsDisks Large Homolog 4 ProteinDouble-Blind MethodFemaleHumansMaleAntipsychotic AgentsBrain-Derived Neurotrophic Factorbryostatin 1BryostatinsDisks Large Homolog 4 ProteinPhosphopyruvate HydrataseProtein Kinase C-epsilonSynaptophysinAlzheimer’s diseasebryostatin 1controlled clinical trialexpanded access trialspharmacokineticsprotein kinase C

Identifiers

PMID28482641
PMCPMC5438479
OpenAlexW2611128115

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.