Evidence map›Paper›PMID 31628598›Full record

ReviewHandbook of experimental pharmacology2020

Translational Molecular Approaches in Substance Abuse Research.

Sasha L Fulton, Ian Maze

Open access · greenAbstract readReview
In one paragraph

Review in Handbook of experimental pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. [Comorbidity of posttraumatic stress disorder and addiction from a biopsychosocial perspective].Neuropsychiatrie : Klinik, Diagnostik, Therapie und Rehabilitation : Organ der Gesellschaft Osterreichischer Nervenarzte und Psychiater · 2022
    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

2 authors at 1 institution in 1 country.

Sasha L FultonDepartment of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Ian MazeDepartment of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ian.maze@mssm.edu.
Icahn School of Medicine at Mount Sinai · US

Funding

Molecular studies of neural histone monoaminylation in normal and aberrant brain plasticityR01MH116900 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ian S. Maze · 2019 to 2026
$4.7M
Training Program in NeuroscienceT32MH087004 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GEORGE W. HUNTLEY · 2009 to 2026
$4.0M
Roles for histone monoaminylation in cocaine-induced transcriptional and behavioral plasticityDP1DA042078 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MAZE, IAN S. · 2016 to 2021
$3.2M
Application of intein-based chemical methods to directly manipulate neuronal histone modifications in rodent models of addictionR21DA044767 · NIDA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DAVID-SHTERNBERG, YAEL E, MAZE, IAN S. · 2018 to 2019
$444k
NIDA NIH HHS DP1 DA042078NIDA NIH HHS R21 DA044767NIMH NIH HHS R01 MH116900NIMH NIH HHS T32 MH087004
6 · The paper itself

Abstract

Excessive abuse of psychoactive substances is one of the leading contributors to morbidity and mortality worldwide. In this book chapter, we review translational research strategies that are applied in the pursuit of new and more effective therapeutics for substance use disorder (SUD). The complex, multidimensional nature of psychiatric disorders like SUD presents difficult challenges to investigators. While animal models are critical for outlining the mechanistic relationships between defined behaviors and genetic and/or molecular changes, the heterogeneous pathophysiology of brain diseases is uniquely human, necessitating the use of human studies and translational research schemes. Translational research describes a cross-species approach in which findings from human patient-based data can be used to guide molecular genetic investigations in preclinical animal models in order to delineate the mechanisms of reward circuitry changes in the addicted state. Results from animal studies can then inform clinical investigations toward the development of novel treatments for SUD. Here we describe the strategies that are used to identify and functionally validate genetic variants in the human genome which may contribute to increased risk for SUD, starting from early candidate gene approaches to more recent genome-wide association studies. We will next examine studies aimed at understanding how transcriptional and epigenetic dysregulation in SUD can persistently alter cellular function in the disease state. In our discussion, we then focus on examples from the literature illustrating molecular genetic methodologies that have been applied to studies of different substances of abuse - from alcohol and nicotine to stimulants and opioids - in order to exemplify how these approaches can both delineate the underlying molecular systems driving drug addiction and provide insights into the genetic basis of SUD.

Indexed as

Translational Research, BiomedicalAnimalsGenome-Wide Association StudyHumansRewardSubstance-Related DisordersEpigeneticsGeneticsMolecular approachesSubstance use disorderTranslational research

Identifiers

PMID31628598
PMCPMC7166137
OpenAlexW2984427394

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.