Evidence map›Paper›PMID 39368113›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

Neuronal hypofunction and network dysfunction in a mouse model at an early stage of tauopathy.

Changyi Ji, Xiaofeng Yang, Mohamed Eleish, Yixiang Jiang, Amber M Tetlow, Soomin C Song, Alejandro Martín-Ávila, Qian Wu, Yanmei Zhou, Wenbiao Gan and 2 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Neuronal hypofunction and network dysfunction in a mouse model at an early stage of tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Changyi JiDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Xiaofeng YangDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Mohamed EleishDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Yixiang JiangDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Amber M TetlowDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Soomin C SongDepartment of Pathology, New York University Grossman School of Medicine, New York, USA.
Alejandro Martín-ÁvilaDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Qian WuDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Yanmei ZhouSkirball Institute, New York University Grossman School of Medicine, New York, USA.
Wenbiao GanSkirball Institute, New York University Grossman School of Medicine, New York, USA.
Yan LinDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.
Einar M SigurdssonDepartment of Neuroscience and Physiology, Neuroscience Institute, New York University Grossman School of Medicine, New York, USA.

Funding

Research Supplement to Promote Diversity in Health-Related ResearchR01AG032611 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Einar M Sigurdsson · 2008 to 2026
$9.7M
Epitope-Specific Targeting of Tau Aggregates.R01NS077239 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Einar M Sigurdsson · 2011 to 2026
$7.9M
Cell-Type Specific Vulnerability to Tauopathy and Its Prevention in Multiple ModelsRF1NS120488 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RYOO, HYUNG D, SIGURDSSON, EINAR M · 2021 to 2021
$2.4M
Cell-Type Specific Vulnerability to Tauopathy and Its Prevention in Multiple ModelsR01NS120488 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RYOO, HYUNG D, SIGURDSSON, EINAR M · 2024 to 2025
$1.6M
Efficacy and Mechanism of Action of Heavy-Chain α-Synuclein Antibody Fragments Derived from LlamaR21AG059391 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SIGURDSSON, EINAR M · 2018 to 2019
$466k
Tau Pathology and Calcium Dyshomeostasis: Novel Imaging Approach and TherapyR21AG069475 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SIGURDSSON, EINAR M · 2020 to 2020
$466k
Alzheimer's Association Research Fellowships AARF-22-924783 (Y.J.)Alzheimer's Association Research Fellowships AARF-22-926735 (C.J.)Alzheimer's Association Research Fellowships AARFD-22-926379 (A.M-A)NIA NIH HHS R01 AG032611NIA NIH HHS R21 AG059391NIA NIH HHS R21 AG069475NIH HHS R01 AG032611NIH HHS R01 NS077239NIH HHS R01 NS120488 (E.M.S.)NIH HHS R21 AG059391NINDS NIH HHS R01 NS077239NINDS NIH HHS R01 NS120488NINDS NIH HHS RF1 NS120488
6 · The paper itself

Abstract

introductionIt is unclear how early neuronal deficits occur in tauopathies, if these are associated with changes in neuronal network activity, and if they can be alleviated with therapies.

methodsTo address this, we performed in vivo two-photon Ca

resultsNeuronal function was impaired at 6 months but did not deteriorate further at 12 months, presumably because cortical tau burden was comparable at these ages. At 6 months, neurons were mostly hypoactive, with enhanced neuronal synchrony, and had dysregulated responses to stimulus. Ex vivo, electrophysiology revealed altered synaptic transmission and enhanced excitability of motor cortical neurons, which likely explains the altered network activity. Acute tau antibody treatment reduced pathological tau and gliosis and partially restored neuronal function. DISCUSSION: Tauopathies are associated with early neuronal deficits that can be attenuated with tau antibody therapy. HIGHLIGHTS: Neuronal hypofunction in awake and behaving mice in early stages of tauopathy. Altered network activity disrupted local circuitry engagement in tauopathy mice. Enhanced neuronal excitability and altered synaptic transmission in tauopathy mice. Tau antibody acutely reduced soluble phospho-tau and improved neuronal function.

Indexed as

Disease Models, AnimalNeuronsTauopathiestau ProteinsAnimalsMaleMiceMice, TransgenicNerve NetSynaptic Transmissiontau Proteinscalcium imagingimmunotherapymouse modelnetwork dysfunctionneuronal hypofunctiontauopathytau proteintwo‐photon imaging

Identifiers

PMID39368113
PMCPMC11567809

What Socratic 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 Socratic graph.