Evidence map›Paper›PMID 21795114›Full record

ReviewTrends in molecular medicine2011

Presenilins in synaptic function and disease.

Angela Ho, Jie Shen

Open access · greenAbstract readReview
In one paragraph

Review in Trends in molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Synaptogenic effect ofScience translational medicine · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Identification of a RareFrontiers in psychiatry · 2020
    Article
  9. Article
  10. The vexing complexity of the amyloidogenic pathway.Protein science : a publication of the Protein Society · 2019
    Review
  11. Bax inhibitor 1 is a γ-secretase-independent presenilin-binding protein.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Article
  13. Article
  14. Role of BACE1 in Alzheimer's synaptic function.Translational neurodegeneration · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Partial loss of presenilin impairs age-dependent neuronal survival in the cerebral cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  19. Synaptic function of nicastrin in hippocampal neurons.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  20. Review
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.

Angela HoDepartment of Biology, Boston University, 5 Cummington Street, Boston MA 02215, USA.
Jie Shen
Boston University · USBrigham and Women's Hospital · US

Funding

Role of Presenilins in the SynapseR01NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI Jie Shen · 2001 to 2026
$10.6M
PS1 &PS2 in Cortical Development and Notch SignalingR01NS042818 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2002 to 2017
$5.7M
Presenilin and APP in the BrainRF1NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2021 to 2021
$2.7M
Mints: Adaptor Proteins Coupling APP of Alzheimer's Disease to the SynapseK01AG027311 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HO, ANGELA · 2006 to 2010
$617k
NIA NIH HHS K01 AG027311NIA NIH HHS K01AG027311NINDS NIH HHS NS041783NINDS NIH HHS NS042818NINDS NIH HHS R01 NS041783NINDS NIH HHS R01 NS042818NINDS NIH HHS RF1 NS041783
6 · The paper itself

Abstract

The presenilin genes harbor approximately 90% of mutations linked to early-onset familial Alzheimer's disease (FAD), but how these mutations cause the disease is still being debated. Genetic analysis in Drosophila and mice demonstrate that presenilin plays essential roles in synaptic function, learning and memory, as well as neuronal survival in the adult brain, and the FAD-linked mutations alter the normal function of presenilin in these processes. Presenilin has also been reported to regulate the calcium homeostasis of intracellular stores, and presynaptic presenilin controls neurotransmitter release and long-term potentiation through modulation of calcium release from intracellular stores. In this review, we highlight recent advances in deciphering the role of presenilin in synaptic function, calcium regulation and disease, and pose key questions for future studies.

Indexed as

Alzheimer DiseaseAnimalsCalciumCerebral CortexHomeostasisHumansMutation, MissensePresenilin-1SynapsesCalciumPresenilin-1

Identifiers

PMID21795114
PMCPMC3205282
OpenAlexW2073660598

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.