Evidence map›Paper›PMID 26724386›Full record

ReviewThe American journal of pathology2016

Dopaminergic Neurons and Brain Reward Pathways: From Neurogenesis to Circuit Assembly.

Sarah X Luo, Eric J Huang

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

88 citing papers in PubMed, 153 citations in OpenAlex.

  1. Identification of Sarmentosin as a Key Bioactive from Blackcurrants (Journal of agricultural and food chemistry · 2024
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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sarah X LuoNeuroscience Graduate Program, University of California San Francisco, San Francisco, California; Department of Pathology, University of California San Francisco, San Francisco, California.
Eric J HuangNeuroscience Graduate Program, University of California San Francisco, San Francisco, California; Department of Pathology, University of California San Francisco, San Francisco, California; Pathology Service 113B, San Francisco Veterans Affairs Medical Center, San Francisco, California. Electronic address: eric.huang2@ucsf.edu.
University of California, San Francisco · US

Funding

Cellular and Animal Models of FUS Mutations in ALSR21OD011915 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2012 to 2013
$421k
Mouse models of neuroprotection in dopamine neuronsK26OD010927 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2012 to 2013
$307k
Mechanisms of ER Stress and Neurodegeneration in Parkinson's DiseaseI01BX001108 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI Eric J Huang · 2011 to 2026
–
Mechanism of FUS Mutations in the Pathogenesis of ALSI21BX001625 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI HUANG, ERIC J · 2013 to 2014
–
BLRD VA I01 BX001108BLRD VA I21 BX001625NIH HHS K26 OD010927NIH HHS OD010927NIH HHS OD011915NIH HHS R21 OD011915
6 · The paper itself

Abstract

Midbrain dopaminergic (DA) neurons in the substantia nigra pars compacta and ventral tegmental area regulate extrapyramidal movement and important cognitive functions, including motivation, reward associations, and habit learning. Dysfunctions in DA neuron circuitry have been implicated in several neuropsychiatric disorders, including addiction and schizophrenia, whereas selective degeneration of DA neurons in substantia nigra pars compacta is a key neuropathological feature in Parkinson disease. Efforts to understand these disorders have focused on dissecting the underlying causes, as well as developing therapeutic strategies to replenish dopamine deficiency. In particular, the promise of cell replacement therapies for clinical intervention has led to extensive research in the identification of mechanisms involved in DA neuron development. It is hoped that a comprehensive understanding of these mechanisms will lead to therapeutic strategies that improve the efficiency of DA neuron production, engraftment, and function. This review provides a comprehensive discussion on how Wnt/β-catenin and sonic hedgehog-Smoothened signaling mechanisms control the specification and expansion of DA progenitors and the differentiation of DA neurons. We also discuss how mechanisms involving transforming growth factor-β and transcriptional cofactor homeodomain interacting protein kinase 2 regulate the survival and maturation of DA neurons in early postnatal life. These results not only reveal fundamental mechanisms regulating DA neuron development, but also provide important insights to their potential contributions to neuropsychiatric and neurodegenerative diseases.

Indexed as

NeurogenesisWnt Signaling PathwayCell DifferentiationDopamineDopaminergic NeuronsHedgehog ProteinsHumansModels, BiologicalMotivationParkinson DiseaseRewardSubstantia NigraVentral Tegmental AreaDopamineHedgehog Proteins

Identifiers

PMID26724386
PMCPMC4816693
OpenAlexW2211023366

What OpenQuestion holds

Textmetadata
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.