Evidence map›Paper›PMID 22285449›Full record

ReviewExperimental neurology2013

Axon degeneration in Parkinson's disease.

Robert E Burke, Karen O'Malley

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 261 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
261citing papers in PubMed, 3 pooled it
10.5field-weighted citation impact, top 1% 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

261 citing papers in PubMed, 3 syntheses or guidelines pooled it, 493 citations in OpenAlex.

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  15. Serotonin Transporter Distribution in the Brainstem of Multiple-System Atrophy-Parkinsonian Type: Insights from Pathology andJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
    Article
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201 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Robert E BurkeDepartment of Neurology, Columbia University, 650 W 168th St., New York, NY, 10032, USA. rb43@columbia.edu
Karen O'Malley
Columbia University · USWashington University in St. Louis · US

Funding

TRANSLATIONAL APPROACHES TO NEUROPROTECTION OF AXONS IN PDrP50NS038370 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 1999 to 2014
$24.0M
APOPTOSIS IN SUBSTANTIA NIGRA FOLLOWING STRIATAL INJURYR01NS026836 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 1994 to 2010
$4.3M
Apoptosis in substantia nigraR56NS026836 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 2011 to 2011
$559k
EFFECT OF PERINATAL ASPHYXIA ON STRIATUMR29NS026836 · NINDS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI BURKE, ROBERT E · 1989 to 1993
–
NINDS NIH HHS NS26836NINDS NIH HHS NS38370NINDS NIH HHS P50 NS038370NINDS NIH HHS R01 NS026836NINDS NIH HHS R56 NS026836
6 · The paper itself

Abstract

Parkinson's disease (PD) is the most common neurodegenerative disease of the basal ganglia. Like other adult-onset neurodegenerative disorders, it is without a treatment that forestalls its chronic progression. Efforts to develop disease-modifying therapies to date have largely focused on the prevention of degeneration of the neuron soma, with the tacit assumption that such approaches will forestall axon degeneration as well. We herein propose that future efforts to develop neuroprotection for PD may benefit from a shift in focus to the distinct mechanisms that underlie axon degeneration. We review evidence from human post-mortem studies, functional neuroimaging, genetic causes of the disease and neurotoxin models that axon degeneration may be the earliest feature of the disease, and it may therefore be the most appropriate target for early intervention. In addition, we present evidence that the molecular mechanisms of degeneration of axons are separate and distinct from those of neuron soma. Progress is being made in understanding these mechanisms, and they provide possible new targets for therapeutic intervention. We also suggest that the potential for axon re-growth in the adult central nervous system has perhaps been underestimated, and it offers new avenues for neurorestoration. In conclusion, we propose that a new focus on the neurobiology of axons, their molecular pathways of degeneration and growth, will offer novel opportunities for neuroprotection and restoration in the treatment of PD and other neurodegenerative diseases.

Indexed as

AnimalsAxonsHumansNerve DegenerationParkinson Disease1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine1-methyl-4-phenylpyridinium[(3)H]TBZOH6-hydroxydopamine6-OHDAAAVADadeno-associated virusAktAlzheimer's diseaseautophagic vacuolesAutophagyAVsdementia with Lewy BodiesDLBILBincidental Lewy bodiesLBleucine rich repeat kinase 2Lewy bodyLRRK2medial forebrain bundleMFBMPP(+)MPTPmTorParkinson's diseasePDSNStriatumsubstantia nigraSubstantia nigraTHtritiated α-dihydrotetrabenazinetyrosine hydroxylasevesicular monoamine transporterVMAT2Wallerian degeneration slowWld(S)α-Synuclein

Identifiers

PMID22285449
PMCPMC3340476
OpenAlexW2070049573

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.