Evidence map›Paper›PMID 33882308›Full record

ArticleCell reports2021

Alzheimer's pathology causes impaired inhibitory connections and reactivation of spatial codes during spatial navigation.

Stephanie M Prince, Abigail L Paulson, Nuri Jeong, Lu Zhang, Solange Amigues, Annabelle C Singer

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Stephanie M PrinceCoulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA 30332, USA; Neuroscience Graduate Program, Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, GA, 30322, USA.
Abigail L PaulsonCoulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA 30332, USA.
Nuri JeongCoulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA 30332, USA; Neuroscience Graduate Program, Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, GA, 30322, USA.
Lu ZhangCoulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA 30332, USA.
Solange AmiguesCoulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA 30332, USA.
Annabelle C SingerCoulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA 30332, USA. Electronic address: asinger@gatech.edu.
Georgia Institute of Technology · US

Funding

The Goizueta Alzheimer's Disease Research CenterP30AG066511 · NIA · EMORY UNIVERSITY · PI Amy D Rodriguez · 2020 to 2026
$29.0M
TRAINING IN TRANSLATIONAL RESEARCH IN NEUROLOGYT32NS007480 · NINDS · EMORY UNIVERSITY · PI LEVEY, ALLAN I · 2000 to 2020
$4.5M
Training In Systems And Integrative Biology NeuroscienceT32NS096050 · NINDS · EMORY UNIVERSITY · PI Yoland Smith · 2016 to 2026
$3.9M
Non-Invasive Methods to Drive Neural Activity with Millisecond Precision and to Recruit the Brain’s Immune CellsR01NS109226 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI Annabelle Catherine Singer · 2018 to 2026
$2.7M
NIA NIH HHS P30 AG066511NINDS NIH HHS R01 NS109226NINDS NIH HHS T32 NS007480NINDS NIH HHS T32 NS096050
6 · The paper itself

Abstract

Synapse loss and altered synaptic strength are thought to underlie cognitive impairment in Alzheimer's disease (AD) by disrupting neural activity essential for memory. While synaptic dysfunction in AD has been well characterized in anesthetized animals and in vitro, it remains unknown how synaptic transmission is altered during behavior. By measuring synaptic efficacy as mice navigate in a virtual reality task, we find deficits in interneuron connection strength onto pyramidal cells in hippocampal CA1 in the 5XFAD mouse model of AD. These inhibitory synaptic deficits are most pronounced during sharp-wave ripples, network oscillations important for memory that require inhibition. Indeed, 5XFAD mice exhibit fewer and shorter sharp-wave ripples with impaired place cell reactivation. By showing inhibitory synaptic dysfunction in 5XFAD mice during spatial navigation behavior and suggesting a synaptic mechanism underlying deficits in network activity essential for memory, this work bridges the gap between synaptic and neural activity deficits in AD.

Indexed as

Alzheimer DiseaseAnimalsBrain WavesCA1 Region, HippocampalDisease Models, AnimalElectrodes, ImplantedHumansInterneuronsMaleMemoryMiceMice, Inbred C57BLMice, TransgenicPyramidal CellsSpatial NavigationSynapses5XFADAlzheimer’s diseaseinhibitioninterneuronsmonosynaptic connectionsneural codingplace cellsreactivationsharp-wave ripples

Identifiers

PMID33882308
PMCPMC8139125
OpenAlexW3154338194

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.