Evidence map›Paper›PMID 26888634›Full record

ArticleScientific reports2016

Abnormal tau induces cognitive impairment through two different mechanisms: synaptic dysfunction and neuronal loss.

J Di, L S Cohen, C P Corbo, G R Phillips, A El Idrissi, A D Alonso

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Tau, atrophy, and domain-specific cognitive impairment in typical Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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  17. Review
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7 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

J DiDepartment of Biology and Center for Developmental Neuroscience, College of Staten Island, City University of New York, Staten Island, NY 10314, USA.
L S CohenDepartment of Biology and Center for Developmental Neuroscience, College of Staten Island, City University of New York, Staten Island, NY 10314, USA.
C P CorboDepartment of Biological Sciences, Wagner College, Staten Island, NY 10301, USA.
G R PhillipsDepartment of Biology and Center for Developmental Neuroscience, College of Staten Island, City University of New York, Staten Island, NY 10314, USA.
A El IdrissiDepartment of Biology and Center for Developmental Neuroscience, College of Staten Island, City University of New York, Staten Island, NY 10314, USA.
A D AlonsoDepartment of Biology and Center for Developmental Neuroscience, College of Staten Island, City University of New York, Staten Island, NY 10314, USA.
College of Staten Island · USCity University of New York · USWagner College · US

Funding

Tau phosphorylation and neurodegenerationR15AG034524 · NIA · COLLEGE OF STATEN ISLAND · PI ALONSO, ALEJANDRA DEL-C · 2009 to 2009
$149k
NIA NIH HHS R15 AG034524NIA NIH HHS R15AG034524-01
6 · The paper itself

Abstract

The hyperphosphorylated microtubule-associated protein tau is present in several neurodegenerative diseases, although the causal relationship remains elusive. Few mouse models used to study Alzheimer-like dementia target tau phosphorylation. We created an inducible pseudophosphorylated tau (Pathological Human Tau, PH-Tau) mouse model to study the effect of conformationally modified tau in vivo. Leaky expression resulted in two levels of PH-Tau: low basal level and higher upon induction (4% and 14% of the endogenous tau, respectively). Unexpectedly, low PH-Tau resulted in significant cognitive deficits, decrease in the number of synapses (seen by EM in the CA1 region), reduction of synaptic proteins, and localization to the nucleus. Induction of PH-Tau triggered neuronal death (60% in CA3), astrocytosis, and loss of the processes in CA1. These findings suggest, that phosphorylated tau is sufficient to induce neurodegeneration and that two different mechanisms can induce cognitive impairment depending on the levels of PH-Tau expression.

Indexed as

Alzheimer DiseaseCA1 Region, HippocampalCognitive DysfunctionGliosisAnimalsCell DeathCell Line, TumorDisease Models, AnimalHumansMiceMice, TransgenicNeuronsPhosphorylationSynapsestau Proteinstau Proteins

Identifiers

PMID26888634
PMCPMC4757872
OpenAlexW2302116106

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.