Evidence map›Paper›PMID 36710361›Full record

ArticleMolecular brain2023

Presenilins regulate synaptic plasticity in the perforant pathways of the hippocampus.

Sang Hun Lee, Vadim Y Bolshakov, Jie Shen

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Cortical neurodegeneration caused byProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Human Presenilin-1 delivered by AAV9 rescues impaired γ-secretase activity, memory deficits, and neurodegeneration inProceedings of the National Academy of Sciences of the United States of America · 2023
    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

3 authors at 2 institutions in 1 country.

Sang Hun LeeDepartment of Neurology, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA. slee82@bwh.harvard.edu.ORCID 0000-0002-0020-4631
Vadim Y BolshakovDepartment of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, 02478, USA.
Jie ShenDepartment of Neurology, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Brigham and Women's Hospital · USHarvard University · US

Funding

Role of Presenilins in the SynapseR01NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI Jie Shen · 2001 to 2026
$10.6M
Cell Type Specific Genomic and Functional Dissection of Fear-Off Amygdala PathwaysR01MH108665 · NIMH · MCLEAN HOSPITAL · PI BOLSHAKOV, VADIM, RESSLER, KERRY J. · 2016 to 2025
$7.5M
Development of novel therapies for FADRF1AG063520 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2019 to 2019
$3.9M
Identification of Presinilin downstream targets in neuronal survivalR01NS101745 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI PERRIMON, NORBERT, SHEN, JIE · 2017 to 2021
$3.6M
Presenilin and APP in the BrainRF1NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2021 to 2021
$2.7M
NIA NIH HHS RF1 AG063520NIMH NIH HHS R01 MH108665NINDS NIH HHS AG063520NINDS NIH HHS NS041783NINDS NIH HHS R01 NS041783NINDS NIH HHS R01 NS101745NINDS NIH HHS RF1 NS041783
6 · The paper itself

Abstract

Mutations in the Presenilin genes (PSEN1 and PSEN2) are the major cause of familial Alzheimer's disease (AD), highlighting the importance of Presenilin (PS) in AD pathogenesis. Previous studies of PS function in the hippocampus demonstrated that loss of PS results in the impairment of short- and long-term synaptic plasticity and neurotransmitter release at hippocampal Schaffer collateral (SC) and mossy fiber (MF) synapses. Cortical input to the hippocampus through the lateral perforant pathway (LPP) and the medial perforant pathway (MPP) is critical for normal cognitive functions and is particularly vulnerable during aging and early stages of AD. Whether PS regulates synaptic function in the perforant pathways, however, remained unknown. In the current study, we investigate PS function in the LPP and MPP by performing whole-cell and field-potential electrophysiological recordings using acute hippocampal slices from postnatal forebrain-restricted excitatory neuron-specific PS conditional double knockout (cDKO) mice. We found that paired-pulse ratio (PPR) is reduced in the LPP and MPP of PS cDKO mice. Moreover, synaptic frequency facilitation or depression in the LPP or MPP, respectively, is impaired in PS cDKO mice. Notably, depletion of intracellular Ca

Indexed as

CalciumPerforant PathwayAnimalsHippocampusLong-Term PotentiationMiceNeuronal PlasticitySynapsesSynaptic TransmissionCalciumAlzheimer’s diseaseCalcium homeostasisConditional knockoutHippocampusLong-term potentiationPerforant pathwaysShort-term synaptic plasticity

Identifiers

PMID36710361
PMCPMC9885562
OpenAlexW4318457250

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.