Evidence map›Paper›PMID 29880815›Full record

ArticleScientific reports2018

Novel interaction between Alzheimer's disease-related protein presenilin 1 and glutamate transporter 1.

Katarzyna Marta Zoltowska, Masato Maesako, Joshua Meier, Oksana Berezovska

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

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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  16. [Progress on loss-of-function hypothesis of presenilin-1 mutations in Alzheimer diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020
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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

4 authors at 1 institution in 2 countries.

Katarzyna Marta ZoltowskaMassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Department of Neurology, 114 16th Street, 02129, Charlestown, MA, USA.ORCID 0000-0001-5853-3465
Masato MaesakoMassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Department of Neurology, 114 16th Street, 02129, Charlestown, MA, USA.
Joshua MeierMassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Department of Neurology, 114 16th Street, 02129, Charlestown, MA, USA.
Oksana BerezovskaMassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Department of Neurology, 114 16th Street, 02129, Charlestown, MA, USA. oberezovska@mgh.harvard.edu.
Harvard University · US

Funding

TRANSGENICS AND PRESENILIN FUNCTIONP01AG015379 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI BEREZOVSKA, OKSANA, SELKOE, DENNIS J · 1998 to 2023
$51.3M
Role of PS1 in neurodegenerationRF1AG044486 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI BEREZOVSKA, OKSANA · 2019 to 2019
$3.2M
Role of PS1 in neurodegenerationR01AG044486 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI BEREZOVSKA, OKSANA · 2014 to 2018
$2.5M
NIA NIH HHS P01 AG015379NIA NIH HHS R01 AG044486NIA NIH HHS RF1 AG044486
6 · The paper itself

Abstract

Neuronal hyperactivity is one of the earliest events observed in Alzheimer's disease (AD). Moreover, alterations in the expression of glutamate transporters have been reported to exacerbate amyloid pathology and cognitive deficits in transgenic AD mouse models. However, the molecular links between these pathophysiological changes remain largely unknown. Here, we report novel interaction between presenilin 1 (PS1), the catalytic component of the amyloid precursor protein-processing enzyme, γ-secretase, and a major glutamate transporter-1 (GLT-1). Our data demonstrate that the interaction occurs between PS1 and GLT-1 expressed at their endogenous levels in vivo and in vitro, takes place in both neurons and astrocytes, and is independent of the PS1 autoproteolysis and γ-secretase activity. This intriguing discovery may shed light on the molecular crosstalk between the proteins linked to the maintenance of glutamate homeostasis and Aβ pathology.

Indexed as

Alzheimer DiseaseAmyloid Precursor Protein SecretasesAnimalsAstrocytesCells, CulturedExcitatory Amino Acid Transporter 2Glutamate Plasma Membrane Transport ProteinsHumansMiceNeuronsPresenilin-1ProteolysisAmyloid Precursor Protein SecretasesExcitatory Amino Acid Transporter 2Glutamate Plasma Membrane Transport ProteinsPresenilin-1presenilin 1, mousePSEN1 protein, humanSLC1A2 protein, humanSlc1a2 protein, mouse

Identifiers

PMID29880815
PMCPMC5992168
OpenAlexW2805822511

What OpenQuestion holds

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Registered trials

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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.