Evidence map›Paper›PMID 33076986›Full record

ArticleActa neuropathologica communications2020

Synaptic and metabolic gene expression alterations in neurons that are recipients of proteopathic tau seeds.

Marta Perez-Rando, Simon Dujardin, Rachel E Bennett, Caitlin Commins, Tara Nibhanupudy, Bradley T Hyman

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 2 institutions in 1 country.

Marta Perez-RandoAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, Building 114, Room 2009, Charlestown, MA, 02129, USA.
Simon DujardinAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, Building 114, Room 2009, Charlestown, MA, 02129, USA.ORCID 0000-0002-5614-341X
Rachel E BennettAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, Building 114, Room 2009, Charlestown, MA, 02129, USA.
Caitlin ComminsAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, Building 114, Room 2009, Charlestown, MA, 02129, USA.
Tara NibhanupudyAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, Building 114, Room 2009, Charlestown, MA, 02129, USA.
Bradley T HymanAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, Building 114, Room 2009, Charlestown, MA, 02129, USA. bhyman@mgh.harvard.edu.ORCID 0000-0002-7959-9401
Harvard University · USMassachusetts General Hospital · US

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Christine S Ritchie · 2019 to 2026
$36.5M
Are multiple tau species toxic in Alzheimer's Disease?RF1AG059789 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2018 to 2018
$2.7M
NIA NIH HHS P30 AG062421NIA NIH HHS RF1 AG059789NIA NIH HHS RF1AG059789-01
6 · The paper itself

Abstract

Recent studies suggest that misfolded tau molecules can be released, and taken up by adjacent neurons, propagating proteopathic seeds across neural systems. Yet critical to understanding whether tau propagation is relevant in pathophysiology of disease would be to learn if it alters neuronal properties. We utilized high resolution multi-color in situ hybridization technology, RNAScope, in a well-established tau transgenic animal, and found that a subset of neurons in the cortex do not appear to express the transgene, but do develop phospho-tau positive inclusions, consistent with having received tau seeds. Recipient neurons show decreases in their expression of synaptophysin, CAMKIIα, and mouse tau in both young and old animals. These results contrast with neurons that develop tau aggregates and also overexpress the transgene, which have few changes in expression of metabolic and synaptic markers. Taken together, these results strongly suggest that tau propagation impacts neuronal functional integrity.

Indexed as

Gene ExpressionAgingAnimalsBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2HumansInclusion BodiesIn Situ HybridizationMiceMice, TransgenicNeuronsRNA, MessengerSynaptophysinTauopathiestau ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mouseMAPT protein, humanMapt protein, mouseRNA, MessengerSynaptophysintau ProteinsAlzheimer’s diseaseNeurofibrillary tanglesRNA expressionTau seeding

Identifiers

PMID33076986
PMCPMC7574323
OpenAlexW3093222995

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.