Evidence map›Paper›PMID 29049003›Full record

ArticleHuman vaccines & immunotherapeutics2018

"Tau immunotherapy: Hopes and hindrances".

Koorosh Shahpasand, Alireza Sepehri Shamloo, Seyed Massood Nabavi, Kun Ping Lu, Xiao Zhen Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Human vaccines & immunotherapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 23 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

5 authors at 2 institutions in 2 countries.

Koorosh Shahpasanda Department of Brain and Cognitive Sciences , Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR , Tehran , Iran.
Alireza Sepehri Shamlooa Department of Brain and Cognitive Sciences , Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR , Tehran , Iran.
Seyed Massood Nabavia Department of Brain and Cognitive Sciences , Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR , Tehran , Iran.
Kun Ping Lub Division of Translational Therapeutics, Department of Medicine , Beth Israel Deaconess Medical Center, Harvard Medical School , Boston , MA , USA.
Xiao Zhen Zhoub Division of Translational Therapeutics, Department of Medicine , Beth Israel Deaconess Medical Center, Harvard Medical School , Boston , MA , USA.
Royan Institute · IRBeth Israel Deaconess Medical Center · US

Funding

Development of Therapeutic Antibody for Traumatic Brain InjuryU01NS096835 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZEIDEL, MARK L. · 2017 to 2021
$5.1M
Role of Tau Conformations in Vascular Contribution to Cognitive Impairment and DementiaR01AG055559 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LO, ENG H., SHEHADAH, AMJAD · 2017 to 2021
$3.4M
Drug Discovery against the Early, Secreted and Toxic Tau in Alzheimer's DiseaseR01AG046319 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LU, KUN PING · 2014 to 2018
$1.8M
NIA NIH HHS R01 AG046319NIA NIH HHS R01 AG055559NINDS NIH HHS U01 NS096835
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurological disorder having two major pathological hallmarks: the extracellular senile plaques and intracellular neurofibrillary tangles composed of amyloid beta protein and hyperphosphorylated tau respectively. Removal of protein deposits from AD brains are the newer attempts for treating AD. The major developments in this direction have been the amyloid and tau based therapeutics. While senile plaque removal employing monoclonal antibodies (mAbs) restore brain function in mouse models of AD, tau has been recently introduced as the major neurodegenerative factor mediating neural cell death. So, several research groups have focused on tau therapy. So far, the outcome of tau immunotherapy has been promising and clearance of hyperphosphorylated tau has been shown to restore the brain function in animal models. But the point is which phosphorylated tau is the most critical form to be removed from the brain, especially because removal of physiologic tau can cause neurodegenerative consequence. Recently, we have shown that phosphorylated tau at Thr231 in the cis conformation is a very early driver of neurodegeneration and cis mAb treatment efficiently restores brain structure and function in TBI models. Because of efficient therapeutic effects in mice model of TBI and considering cis pT231-tau accumulation in AD brains, it could be a very good candidate for tau immunotherapy upon several tauopathy disorders including AD.

Indexed as

ImmunotherapyAlzheimer DiseaseAnimalsDenervationHumanstau ProteinsTreatment Outcometau ProteinsAzheimer's diseaseBeta amyloidCis pT231-tauImmunotherapyTau phosphorylation

Identifiers

PMID29049003
PMCPMC5806642
OpenAlexW2766438782

What OpenQuestion holds

Textmetadata
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.