Evidence map›Paper›PMID 28540422›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2018

Loss and remodeling of striatal dendritic spines in Parkinson's disease: from homeostasis to maladaptive plasticity?

Rosa M Villalba, Yoland Smith

Abstract readReview
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 91 citations in OpenAlex.

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  13. Adenosine AInternational journal of molecular sciences · 2024
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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

2 authors at 1 institution in 1 country.

Rosa M VillalbaYerkes National Primate Research Center, Emory University, 954 Gatewood Rd. NE, Atlanta, GA, 30329, USA. rvillal@emory.edu.ORCID 0000-0001-6156-3606
Yoland SmithYerkes National Primate Research Center, Emory University, 954 Gatewood Rd. NE, Atlanta, GA, 30329, USA.
Emory University · US

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
Udall Parkinson's Disease Research Center at Emory UniversityP50NS098685 · NINDS · EMORY UNIVERSITY · PI SMITH, YOLAND · 2016 to 2020
$6.7M
Thalamic interactions with the striatumR01NS083386 · NINDS · EMORY UNIVERSITY · PI WICHMANN, THOMAS · 2013 to 2017
$2.1M
NIH HHS P50NS098685NIH HHS P51 OD011132NINDS NIH HHS P50 NS098685NINDS NIH HHS R01 NS083386
6 · The paper itself

Abstract

In Parkinson's disease (PD) patients and animal models of PD, the progressive degeneration of the nigrostriatal dopamine (DA) projection leads to two major changes in the morphology of striatal projection neurons (SPNs), i.e., a profound loss of dendritic spines and the remodeling of axospinous glutamatergic synapses. Striatal spine loss is an early event tightly associated with the extent of striatal DA denervation, but not the severity of parkinsonian motor symptoms, suggesting that striatal spine pruning might be a form of homeostatic plasticity that compensates for the loss of striatal DA innervation and the resulting dysregulation of corticostriatal glutamatergic transmission. On the other hand, the remodeling of axospinous corticostriatal and thalamostriatal glutamatergic synapses might represent a form of late maladaptive plasticity that underlies changes in the strength and plastic properties of these afferents and the resulting increased firing and bursting activity of striatal SPNs in the parkinsonian state. There is also evidence that these abnormal synaptic connections might contribute to the pathophysiology of L-DOPA-induced dyskinesia. Despite the significant advances made in this field over the last thirty years, many controversial issues remain about the striatal SPN subtypes affected, the role of spine changes in the altered activity of SPNs in the parkinsonisn state, and the importance of striatal spine plasticity in the pathophysiology of L-DOPA-induced dyskinesia. In this review, we will examine the current state of knowledge of these issues, discuss the limitations of the animal models used to address some of these questions, and assess the relevance of data from animal models to the human-diseased condition.

Indexed as

AnimalsCorpus StriatumDendritic SpinesDisease Models, AnimalHaplorhiniHomeostasisNeuronal PlasticityParkinson DiseaseCorticostriatalDopamineGlutamateMonkeyStriatumThalamostriatal

Identifiers

PMID28540422
PMCPMC5701884
OpenAlexW2617325570

What OpenQuestion holds

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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.