Evidence map›Paper›PMID 19527737›Full record

ReviewLife sciences2010

Enhancement of endocannabinoid signaling by fatty acid amide hydrolase inhibition: a neuroprotective therapeutic modality.

Jeannie Hwang, Crista Adamson, David Butler, David R Janero, Alexandros Makriyannis, Ben A Bahr

Abstract readReview
In one paragraph

Review in Life sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Ageing, Neurodegeneration and the Endocannabinoid System.Current topics in behavioral neurosciences · 2026
    Review
  2. Exceptionally Potent Chiral Anandamide Analogs.Journal of medicinal chemistry · 2025
    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

6 authors.

Jeannie HwangDepartment of Pharmaceutical Sciences and the Neurosciences Program, University of Connecticut, Storrs, Connecticut, USA.
Crista Adamson
David Butler
David R Janero
Alexandros Makriyannis
Ben A Bahr

Funding

Training Program in Medications Development for Drugs of Abuse (Institutional RutT32DA007312 · NIDA · UNIVERSITY OF CONNECTICUT STORRS · PI MAKRIYANNIS, ALEXANDROS · 1999 to 2013
$4.1M
NIDA NIH HHS T32 DA007312
6 · The paper itself

Abstract

aimsThis review posits that fatty acid amide hydrolase (FAAH) inhibition has therapeutic potential against neuropathological states including traumatic brain injury; Alzheimer's, Huntington's, and Parkinson's diseases; and stroke. MAIN

methodsThis proposition is supported by data from numerous in vitro and in vivo experiments establishing metabolic and pharmacological contexts for the neuroprotective role of the endogenous cannabinoid ("endocannabinoid") system and selective FAAH inhibitors. KEY

findingsThe systems biology of endocannabinoid signaling involves two main cannabinoid receptors, the principal endocannabinoid lipid mediators N-arachidonoylethanolamine ("anandamide") (AEA) and 2-arachidonoyl glycerol (2-AG), related metabolites, and the proteins involved in endocannabinoid biosynthesis, biotransformation, and transit. The endocannabinoid system is capable of activating distinct signaling pathways on-demand in response to pathogenic events or stimuli, thereby enhancing cell survival and promoting tissue repair. Accumulating data suggest that endocannabinoid system modulation at discrete targets is a promising pharmacotherapeutic strategy for treating various medical conditions. In particular, neuronal injury activates cannabinoid signaling in the central nervous system as an intrinsic neuroprotective response. Indirect potentiation of this salutary response through pharmacological inhibition of FAAH, an endocannabinoid-deactivating enzyme, and consequent activation of signaling pathways downstream from cannabinoid receptors have been shown to promote neuronal maintenance and function. SIGNIFICANCE: This therapeutic modality has the potential to offer site- and event-specific neuroprotection under conditions where endocannabinoids are being produced as part of a physiological protective mechanism. In contrast, direct application of cannabinoid receptor agonists to the central nervous system may activate CB receptors indiscriminately and invite unwanted psychotrophic effects.

Indexed as

EndocannabinoidsAmidohydrolasesAnimalsCannabinoid Receptor ModulatorsDrug Delivery SystemsFatty Acid Amide HydrolasesHumansNervous System DiseasesNeurodegenerative DiseasesNeuroprotective AgentsSignal TransductionAmidohydrolasesCannabinoid Receptor ModulatorsEndocannabinoidsFatty Acid Amide HydrolasesNeuroprotective Agents

Identifiers

PMID19527737
PMCPMC2848893

What OpenQuestion holds

Textmetadata
LicenceTDM
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.