Evidence map›Paper›PMID 23382994›Full record

ArticlePloS one2013

Neurotrophic and neuroprotective actions of (-)- and (+)-phenserine, candidate drugs for Alzheimer's disease.

Anna M Lilja, Yu Luo, Qian-sheng Yu, Jennie Röjdner, Yazhou Li, Ann M Marini, Amelia Marutle, Agneta Nordberg, Nigel H Greig

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. ACS pharmacology & translational science · 2022
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Hexahydropyrrolo[2,3-ACS chemical neuroscience · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. Alzheimer's Disease and Its Potential Alternative Therapeutics.Journal of Alzheimer's disease & Parkinsonism · 2019
    Article
  17. Does traumatic brain injury hold the key to the Alzheimer's disease puzzle?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2018
    Review
  18. Article
  19. Article
  20. Article
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

9 authors at 6 institutions in 2 countries.

Anna M LiljaAlzheimer Neurobiology Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden. anna.lilja@ki.se
Yu Luo
Qian-sheng Yu
Jennie Röjdner
Yazhou Li
Ann M Marini
Amelia Marutle
Agneta Nordberg
Nigel H Greig
Karolinska Institutet · SENational Institute on Aging · USNational Institutes of Health · USKarolinska University Hospital · SEUniformed Services University of the Health Sciences · USUniversity School · US

Funding

Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Neuronal dysfunction and demise together with a reduction in neurogenesis are cardinal features of Alzheimer's disease (AD) induced by a combination of oxidative stress, toxic amyloid-β peptide (Aβ) and a loss of trophic factor support. Amelioration of these was assessed with the Aβ lowering AD experimental drugs (+)-phenserine and (-)-phenserine in neuronal cultures, and actions in mice were evaluated with (+)-phenserine. Both experimental drugs together with the metabolite N1-norphenserine induced neurotrophic actions in human SH-SY5Y cells that were mediated by the protein kinase C (PKC) and extracellular signal-regulated kinases (ERK) pathways, were evident in cells expressing amyloid precursor protein Swedish mutation (APP(SWE)), and retained in the presence of Aβ and oxidative stress challenge. (+)-Phenserine, together with its (-) enantiomer as well as its N1- and N8-norphenserine and N1,N8-bisnorphenserine metabolites, likewise provided neuroprotective activity against oxidative stress and glutamate toxicity via the PKC and ERK pathways. These neurotrophic and neuroprotective actions were evident in primary cultures of subventricular zone (SVZ) neural progenitor cells, whose neurosphere size and survival were augmented by (+)-phenserine. Translation of these effects in vivo was assessed in wild type and AD APPswe transgenic (Tg2576) mice by doublecortin (DCX) immunohistochemical analysis of neurogenesis in the SVZ, which was significantly elevated by 16 day systemic (+)-phenserine treatment, in the presence of a (+)-phenserine-induced elevation in brain- derived neurotrophic factor (BDNF).

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCell Line, TumorCell ProliferationDose-Response Relationship, DrugDoublecortin ProteinDrug DiscoveryGene Expression RegulationHumansMiceMice, TransgenicMutationNeural Stem CellsNeuronsAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorDcx protein, mouseDoublecortin ProteinNeuroprotective AgentsPeptide FragmentsphenserinePhysostigmine

Identifiers

PMID23382994
PMCPMC3559887
OpenAlexW2045139734

What OpenQuestion holds

Textmetadata
LicenceCC0
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.