Evidence map›Paper›PMID 32822389›Full record

ArticlePLoS biology2020

Chemogenetic attenuation of neuronal activity in the entorhinal cortex reduces Aβ and tau pathology in the hippocampus.

Gustavo A Rodriguez, Geoffrey M Barrett, Karen E Duff, S Abid Hussaini

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06864910 (Brain Connectivity in Mild Cognitive Impairment and Alzheimer's Disease), which is not on this map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 4% 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.

NCT06864910 completednot on this map

Brain Connectivity in Mild Cognitive Impairment and Alzheimer's Disease: A Resting and Task-based fMRI-MEG Study Examining Alterations in Functional Connectivity Following Treatment With Transcranial Current Stimulation (tDCS)

TypeobservationalSponsorNational Institute of Mental Health and Neuro Sciences, IndiaRan2019 to 2022Enrolled40ConditionsCognitive ImpairmentArmsanodal transcranial Direct Current Stimulation
3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  4. Excitation-inhibition homeostasis in Alzheimer's disease: a selective multiscale review of mechanisms, sex differences, and therapeutic opportunities.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
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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.

Gustavo A RodriguezTaub Institute for Research on Alzheimer's disease and the Aging Brain, Columbia University Irving Medical Center, New York, New York, United States of America.ORCID 0000-0003-1307-0297
Geoffrey M BarrettTaub Institute for Research on Alzheimer's disease and the Aging Brain, Columbia University Irving Medical Center, New York, New York, United States of America.ORCID 0000-0001-5129-6348
Karen E DuffTaub Institute for Research on Alzheimer's disease and the Aging Brain, Columbia University Irving Medical Center, New York, New York, United States of America.ORCID 0000-0002-6177-868X
S Abid HussainiTaub Institute for Research on Alzheimer's disease and the Aging Brain, Columbia University Irving Medical Center, New York, New York, United States of America.ORCID 0000-0002-3921-9021
Columbia University Irving Medical Center · US

Funding

Electrophysiological Evaluation of Brain Regions Vulnerable to Alzheimers DiseaseR01AG064066 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HUSSAINI, S. ABID · 2020 to 2024
$4.2M
Entorhinal-hippocampal circuit dysfunction in AD miceR01AG050425 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HUSSAINI, S. ABID · 2015 to 2019
$2.5M
Medical Research CouncilNIA NIH HHS R01 AG050425NIA NIH HHS R01 AG064066
6 · The paper itself

Abstract

High levels of the amyloid-beta (Aβ) peptide have been shown to disrupt neuronal function and induce hyperexcitability, but it is unclear what effects Aβ-associated hyperexcitability may have on tauopathy pathogenesis or propagation in vivo. Using a novel transgenic mouse line to model the impact of human APP (hAPP)/Aβ accumulation on tauopathy in the entorhinal cortex-hippocampal (EC-HIPP) network, we demonstrate that hAPP overexpression aggravates EC-Tau aggregation and accelerates pathological tau spread into the hippocampus. In vivo recordings revealed a strong role for hAPP/Aβ, but not tau, in the emergence of EC neuronal hyperactivity and impaired theta rhythmicity. Chronic chemogenetic attenuation of EC neuronal hyperactivity led to reduced hAPP/Aβ accumulation and reduced pathological tau spread into downstream hippocampus. These data strongly support the hypothesis that in Alzheimer's disease (AD), Aβ-associated hyperactivity accelerates the progression of pathological tau along vulnerable neuronal circuits, and demonstrates the utility of chronic, neuromodulatory approaches in ameliorating AD pathology in vivo.

Indexed as

Action PotentialsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2DependovirusDisease Models, AnimalElectrodes, ImplantedEntorhinal CortexFemaleGene Expression RegulationGenetic VectorsHippocampusHumansMaleMiceAmyloid beta-Protein PrecursorAPP protein, humanCalcium-Calmodulin-Dependent Protein Kinase Type 2Protein Aggregatestau Proteins

Identifiers

PMID32822389
PMCPMC7467290
OpenAlexW3081507804

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.