Evidence map›Paper›PMID 30808415›Full record

ArticleActa neuropathologica communications2019

Tau as a mediator of neurotoxicity associated to cerebral amyloid angiopathy.

Yingjian You, Abigail Perkins, Pablo Cisternas, Braulio Muñoz, Xavier Taylor, Yanwen You, Holly J Garringer, Adrian L Oblak, Brady K Atwood, Ruben Vidal and 1 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  5. Tau depletion diminishes vascular amyloid-related deficits in a mouse model of cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

11 authors at 2 institutions in 1 country.

Yingjian YouStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Abigail PerkinsStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Pablo CisternasStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Braulio MuñozStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Xavier TaylorStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Yanwen YouStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Holly J GarringerDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Adrian L OblakStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Brady K AtwoodStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Ruben VidalStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Cristian A Lasagna-ReevesStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. clasagna@iu.edu.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Comprehensive identification and validation of immune and inflammatory signatures associated to Cerebral Amyloid Angiopathy (CAA) utilizing the NanoString technology.R01AG059639 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LASAGNA-REEVES, CRISTIAN · 2018 to 2022
$3.1M
Studying the Physiological Role of Nuak1 in Tau PathogenesisK22NS092688 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI LASAGNA-REEVES, CRISTIAN · 2015 to 2019
$938k
Dorsal striatal mu opioid receptor function and alcohol useR00AA023507 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI ATWOOD, BRADY · 2016 to 2018
$686k
Alzheimer's Association AARGD-591887NIAAA NIH HHS R00 AA023507NIA NIH HHS R01 AG059639NINDS NIH HHS K22 NS092688
6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there is no clear understanding of the mechanisms underlying the contribution of CAA to neurodegeneration. Despite the fact that CAA is highly associated with accumulation of Aβ, other types of amyloids have been shown to associate with the vasculature. Interestingly, in many cases, vascular amyloidosis is accompanied by significant tau pathology. However, the contribution of tau to neurodegeneration associated to CAA remains to be determined. We used a mouse model of Familial Danish Dementia (FDD), a neurodegenerative disease characterized by the accumulation of Danish amyloid (ADan) in the vasculature, to characterize the contribution of tau to neurodegeneration associated to CAA. We performed histological and biochemical assays to establish tau modifications associated with CAA in conjunction with cell-based and electrophysiological assays to determine the role of tau in the synaptic dysfunction associated with ADan. We demonstrated that ADan aggregates induced hyperphosphorylation and misfolding of tau. Moreover, in a mouse model for CAA, we observed tau oligomers closely associated to astrocytes in the vicinity of vascular amyloid deposits. We finally determined that the absence of tau prevents synaptic dysfunction induced by ADan oligomers. In addition to demonstrating the effect of ADan amyloid on tau misfolding, our results provide compelling evidence of the role of tau in neurodegeneration associated with ADan-CAA and suggest that decreasing tau levels could be a feasible approach for the treatment of CAA.

Indexed as

Amino Acid SequenceAmyloidosisAnimalsCataractCerebellar AtaxiaCerebral Amyloid AngiopathyDeafnessDementiaFemaleHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, Transgenictau ProteinsADan oligomersCerebral amyloid angiopathyNeurodegenerationTau downregulationTau oligomersVascular amyloid

Identifiers

PMID30808415
PMCPMC6390363
OpenAlexW2915481512

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.