Evidence map›Paper›PMID 31864759›Full record

ArticleNeurobiology of aging2020

Presenilin 1 increases association with synaptotagmin 1 during normal aging.

Laura J Keller, Nicole M Sekula, Sarah Svirsky, Masato Maesako, Katarzyna M Zoltowska, Oksana Berezovska

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

Article in Neurobiology of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Primary Hypothyroidism and Alzheimer's Disease: A Tale of Two.Cellular and molecular neurobiology · 2023
    Review
  3. 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

6 authors at 1 institution in 1 country.

Laura J KellerAlzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Nicole M SekulaAlzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Sarah SvirskyAlzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Masato MaesakoAlzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Katarzyna M ZoltowskaAlzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Oksana BerezovskaAlzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA. Electronic address: 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

Presenilin 1 (PS1), the catalytic component of gamma secretase, associates with synaptotagmin 1 (Syt-1). This interaction is decreased in the brains of patients with sporadic Alzheimer's disease. However, it remains unclear how this interaction changes during normal aging. Because aging is a risk factor for Alzheimer's disease, we sought to identify changes in PS1 and Syt-1 association during aging in primary neurons in vitro and mouse brain sections ex vivo. We also tested the effect of aging on the calcium dependence of the interaction by treating neurons aged in vitro with KCl. We found that PS1 and Syt-1 increase their association with age, an effect that is more robust in neuronal processes than cell bodies. Treatment with KCl triggered the interaction in both young and old neurons. Baseline calcium levels and calcium influx in response to KCl treatment were significantly higher in older neurons, which can partially explain the increase in PS1/Syt-1 binding with age. These results suggest a compensatory mechanism during normal aging to offset detrimental age-associated effects.

Indexed as

Alzheimer DiseaseAmyloid Precursor Protein SecretasesAnimalsBrainCalciumCells, CulturedFemaleHealthy AgingHumansMice, Inbred C57BLPotassium ChloridePresenilin-1Protein BindingSynaptotagmin IAmyloid Precursor Protein SecretasesCalciumPotassium ChloridePresenilin-1presenilin 1, mouseSynaptotagmin ISyt1 protein, mouseAgingAlzheimer's diseaseGamma secretaseNeurosciencePresenilin 1Synaptotagmin 1

Identifiers

PMID31864759
PMCPMC7325863
OpenAlexW2982786342

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.