Evidence map›Paper›PMID 36702318›Full record

ArticleNeurobiology of disease2023

Overexpression of alpha synuclein disrupts APP and Endolysosomal axonal trafficking in a mouse model of synucleinopathy.

Suzhen Lin, André D G Leitão, Savannah Fang, Yingli Gu, Sophia Barber, Rhiannon Gilliard-Telefoni, Alfredo Castro, Kijung Sung, Ruinan Shen, Jazmin B Florio and 6 more

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. The Biological Activity ofMolecules (Basel, Switzerland) · 2024
    Review
  9. Article
  10. 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

16 authors at 4 institutions in 2 countries.

Suzhen LinInstitute of Neurology, Ruijing Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China; Department of Neurosciences, University of California San Diego, La Jolla, CA, USA.
André D G LeitãoDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Savannah FangDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Yingli GuDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Sophia BarberDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Rhiannon Gilliard-TelefoniDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Alfredo CastroDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Kijung SungDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Ruinan ShenInstitute of Neurology, Ruijing Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China; Department of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Jazmin B FlorioDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Michael L ManteDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Jianqing DingInstitute of Neurology, Ruijing Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Brian SpencerDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Eliezer MasliahDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Robert A RissmanDepartment of Neurosciences, University of California San Diego, La Jolla, CA, USA; VA San Diego Health System, La Jolla, CA, USA. Electronic address: rrissman@health.ucsd.edu.
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 · CNRuijin Hospital · CNUC San Diego Health System · US

Funding

UCSD Shiley-Marcos Alzheimer's Disease Research Center P30P30AG062429 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Steven Dyal Edland · 2019 to 2026
$34.9M
USCADRC Diversity Supplement PachicanoP30AG066530 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HELENA Chang CHUI, ARTHUR W TOGA · 2020 to 2026
$27.8M
Project 3: TRiC modulation of CNS pathogenesis in HD mouse modelsP01NS092525 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI THOMPSON, LESLIE MICHELS · 2016 to 2020
$6.3M
B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
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
Precision Medicine for Inflammatory Treatment for Alzheimer's Disease in Down SyndromeRF1AG073979 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RAFII, MICHAEL S, RISSMAN, ROBERT · 2021 to 2022
$2.6M
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
Precision Medicine for Inflammatory Treatment for Alzheimer's Disease in Down SyndromeR01AG073979 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RAFII, MICHAEL S, RISSMAN, ROBERT · 2024 to 2025
$1.2M
NIA NIH HHS P30 AG062429NIA NIH HHS P30 AG066530NIA NIH HHS R01 AG018440NIA NIH HHS R01 AG073979NIA NIH HHS R37 AG018440NIA NIH HHS RF1 AG072053NIA NIH HHS RF1 AG073979NINDS NIH HHS P01 NS092525
6 · The paper itself

Abstract

Mutations or triplication of the alpha synuclein (ASYN) gene contribute to synucleinopathies including Parkinson's disease (PD), Dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Recent evidence suggests that ASYN also plays an important role in amyloid-induced neurotoxicity, although the mechanism(s) remains unknown. One hypothesis is that accumulation of ASYN alters endolysosomal pathways to impact axonal trafficking and processing of the amyloid precursor protein (APP). To define an axonal function for ASYN, we used a transgenic mouse model of synucleinopathy that expresses a GFP-human ASYN (GFP-hASYN) transgene and an ASYN knockout (ASYN

Indexed as

Parkinson DiseaseSynucleinopathiesalpha-SynucleinAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesHumansLysosomesMiceMice, Transgenicalpha-SynucleinAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesAlpha synucleinAlzheimer's diseaseAPPAxonal traffickingbeta amyloidLysosomesMitochondriaParkinson's diseaseRab5Rab7

Identifiers

PMID36702318
PMCPMC10754494
OpenAlexW4317754253

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.