Evidence map›Paper›PMID 19889130›Full record

ReviewCNS neuroscience & therapeutics2009

Potential mechanisms involved in the prevention of neurodegenerative diseases by lithium.

Antoni Camins, Ester Verdaguer, Felix Junyent, Marc Yeste-Velasco, Carme Pelegrí, Jordi Vilaplana, Mercé Pallás

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02129348 (Treatment of Psychosis and Agitation in Alzheimer's Disease), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 11% 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.

NCT02129348 phase2completednot on this mapstarted 2014, after this paper: background citation

Treatment of Psychosis and Agitation in Alzheimer's Disease

TypeinterventionalSponsorNew York State Psychiatric InstituteRan2014 to 2020Enrolled77ConditionsAlzheimer's Disease, Psychosis, AgitationArmsLithium, Placebo
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Neuroprotective effect of lithium after pilocarpine-induced status epilepticus in mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Lithium: a versatile tool for understanding renal physiology.American journal of physiology. Renal physiology · 2013
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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.

Antoni CaminsUnitat de Farmacologia i Farmacognòsia Facultat de Farmàcia, Centros de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Institut de Biomedicina (IBUB). Universitat de Barcelona, Barcelona, Spain. camins@ub.edu
Ester Verdaguer
Felix Junyent
Marc Yeste-Velasco
Carme Pelegrí
Jordi Vilaplana
Mercé Pallás
Biomedical Research Networking Center on Neurodegenerative Diseases · ESCentro de Investigación Biomédica en Red · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lithium is a monovalent cation that was introduced in 1949 by John Cade for the treatment of bipolar disorder. Clinical reports and subsequent studies confirmed this application and the beneficial effects of this compound. However, over the last 15 years, various authors have also demonstrated the neuroprotective effects of lithium against several neurotoxic paradigms. Thus, experimental studies in neuronal cell cultures and animal models of Alzheimer disease and others pathologies have provided strong evidence for the potential benefits of lithium. The main mechanism underlying its neuroprotective effects is thought to be inhibition of glycogen synthase kinase-3 (GSK-3), although other biochemical pathways in the brain could also be affected. In this review, the main mechanisms of lithium action are summarized, including the modulation of glutamate receptors, effects on arachidonic acid metabolism, its role with respect to AKT, and other potential mechanisms. In addition, its effects on neuroprotective proteins such as Bcl-2 and p53 are also discussed. Although the cellular and molecular biological effects of lithium may constitute an effective therapeutic strategy for Alzheimer disease, further clinical and experimental studies with this drug and specific GSK-3 inhibitors are necessary to confirm the use of lithium in therapeutic approaches to neurodegenerative diseases.

Indexed as

AnimalsAutophagyGlycogen Synthase Kinase 3HumansLithium CompoundsModels, BiologicalNerve Growth FactorNeurodegenerative DiseasesNeuroprotective AgentsOxidative StressGlycogen Synthase Kinase 3Lithium CompoundsNerve Growth FactorNeuroprotective Agents

Identifiers

PMID19889130
PMCPMC6494035
OpenAlexW2051251797

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.