Evidence map›Paper›PMID 32693191›Full record

ArticleProgress in neurobiology2020

A missense point mutation in nerve growth factor (NGF

Wanlin Yang, Kijung Sung, Wei Xu, Maria J Rodriguez, Andrew C Wu, Sarai A Santos, Savannah Fang, Rebecca K Uber, Stephanie X Dong, Brandon C Guillory and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Progress in neurobiology, 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
0.5field-weighted citation impact, top 42% 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, 7 citations in OpenAlex.

  1. Review
  2. 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

17 authors at 2 institutions in 2 countries.

Wanlin YangDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Neurosciences, University of California San Diego, La Jolla, CA, USA; Department of Neurology, Zhuijiang Hospital, Southern Medical University, Guangzhou, China.
Kijung SungDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Wei XuDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Maria J RodriguezDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA; Department of Pathology, University of California San Diego, La Jolla, CA, USA.
Andrew C WuDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Sarai A SantosDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Savannah FangDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Rebecca K UberDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Stephanie X DongDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Brandon C GuilloryDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Xavier OrainDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Jordan RausDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Corrine JolivaltDepartment of Pathology, University of California San Diego, La Jolla, CA, USA.
Nigel CalcuttDepartment of Pathology, University of California San Diego, La Jolla, CA, USA.
Robert A RissmanDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA; Veterans Affairs San Diego Healthcare System, San Diego, CA, USA.
Jianqing DingDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chengbiao WuDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA. Electronic address: chw049@ucsd.edu.
University of California, San Diego · USShanghai Jiao Tong University · CN

Funding

B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
Novel Systemic Delivery of Peptide-Mediated Anti-Sense Oligonucleotides for Dementia with Lewy BodiesRF1AG072053 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2021 to 2021
$1.8M
Cholinergic constraint and diabetic neuropathyR01NS081082 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CALCUTT, NIGEL A. · 2013 to 2017
$1.6M
Comorbidity of Alzheimer's disease and Diabetes: pathologic mechanism and therapyR01AG039736 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JOLIVALT, CORINNE · 2011 to 2015
$1.6M
Pathogenicity of neuronally-derived tau in exosomesR21AG051839 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2016 to 2017
$426k
BLRD VA I01 BX003040NIA NIH HHS R01 AG018440NIA NIH HHS R01 AG039736NIA NIH HHS R21 AG051839NIA NIH HHS R37 AG018440NIA NIH HHS RF1 AG072053NINDS NIH HHS R01 NS081082
6 · The paper itself

Abstract

The R100W mutation in nerve growth factor is associated with hereditary sensory autonomic neuropathy V in a Swedish family. These patients develop severe loss of perception to deep pain but with apparently normal cognitive functions. To better understand the disease mechanism, we examined a knockin mouse model of HSAN V. The homozygous mice showed significant structural deficits in intra-epidermal nerve fibers (IENFs) at birth. These mice had a total loss of pain perception at ∼2 months of age and often failed to survive to adulthood. Heterozygous mutant mice developed a progressive degeneration of small sensory fibers both behaviorally and functionally: they showed a progressive loss of IENFs starting at the age of 9 months accompanied with progressive loss of perception to painful stimuli such as noxious temperature. Quantitative analysis of lumbar 4/5 dorsal root ganglia revealed a significant reduction in small size neurons, while analysis of sciatic nerve fibers revealed the heterozygous mutant mice had no reduction in myelinated nerve fibers. Significantly, the amount of NGF secreted from mouse embryonic fibroblasts were reduced from both heterozygous and homozygous mice compared to their wild-type littermates. Interestingly, the heterozygous mice showed no apparent structural alteration in the brain: neither the anterior cingulate cortex nor the medial septum including NGF-dependent basal forebrain cholinergic neurons. Accordingly, these animals did not develop appreciable deficits in tests for brain function. Our study has thus demonstrated that the NGF

Indexed as

AnimalsBehavior, AnimalDisease Models, AnimalDisease ProgressionEmbryo, MammalianFibroblastsHereditary Sensory and Autonomic NeuropathiesHeterozygoteHomozygoteLearningMiceMice, TransgenicMutation, MissenseNerve Growth FactorPain PerceptionPoint MutationNerve Growth FactorNGF protein, humanCognitionDorsal root ganglionHereditary sensory autonomic neuropathy VIntraepidermal nerve fiberKnockin mouse modelNerve growth factorNociceptionp75 neutrophic factor receptorPainTrkA

Identifiers

PMID32693191
PMCPMC12327444
OpenAlexW3042382727

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.