Evidence map›Paper›PMID 23372648›Full record

ArticlePloS one2013

Accumulation of intraneuronal β-amyloid 42 peptides is associated with early changes in microtubule-associated protein 2 in neurites and synapses.

Reisuke H Takahashi, Estibaliz Capetillo-Zarate, Michael T Lin, Teresa A Milner, Gunnar K Gouras

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

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  12. The NaFrontiers in pharmacology · 2021
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  17. TOM1 Regulates Neuronal Accumulation of Amyloid-β Oligomers by FcγRIIb2 Variant in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  18. Review
  19. Article
  20. Regulation of Synaptic Amyloid-β Generation through BACE1 Retrograde Transport in a Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

5 authors at 2 institutions in 3 countries.

Reisuke H TakahashiDepartment of Anatomic Pathology, Tokyo Medical University, Tokyo, Japan. takaharh@tokyo-med.ac.jp
Estibaliz Capetillo-Zarate
Michael T Lin
Teresa A Milner
Gunnar K Gouras
Cornell University · USTokyo Medical University · JP

Funding

REGULATION OF CEREBRAL BLOOD FLOW BY THE ROSTRAL VENTROLATERAL MEDULLAP01HL018974 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MILNER, TERESA A · 1985 to 2008
$12.1M
ULTRASTRUCTURAL INTERACTIONS OF OPIOIDS IN HIPPOCAMPUSR01DA008259 · NIDA · WEILL MEDICAL COLL OF CORNELL UNIV · PI MILNER, TERESA A · 1993 to 2019
$6.4M
The Subcellular Neuropathology of Alzheimer's DiseaseR01NS045677 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI GOURAS, GUNNAR K · 2003 to 2007
$1.1M
BIOLOGY OF ALZHEIMER AMYLOID IN NEURONSK02AG028174 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI GOURAS, GUNNAR K · 2006 to 2010
$532k
NHLBI NIH HHS HL18974NHLBI NIH HHS P01 HL018974NIA NIH HHS AG028174NIA NIH HHS K02 AG028174NIDA NIH HHS DA08259NIDA NIH HHS R01 DA008259NINDS NIH HHS NS045677NINDS NIH HHS R01 NS045677
6 · The paper itself

Abstract

Pathologic aggregation of β-amyloid (Aβ) peptide and the axonal microtubule-associated protein tau protein are hallmarks of Alzheimer's disease (AD). Evidence supports that Aβ peptide accumulation precedes microtubule-related pathology, although the link between Aβ and tau remains unclear. We previously provided evidence for early co-localization of Aβ42 peptides and hyperphosphorylated tau within postsynaptic terminals of CA1 dendrites in the hippocampus of AD transgenic mice. Here, we explore the relation between Aβ peptide accumulation and the dendritic, microtubule-associated protein 2 (MAP2) in the well-characterized amyloid precursor protein Swedish mutant transgenic mouse (Tg2576). We provide evidence that localized intraneuronal accumulation of Aβ42 peptides is spatially associated with reductions of MAP2 in dendrites and postsynaptic compartments of Tg2576 mice at early ages. Our data support that reduction in MAP2 begins at sites of Aβ42 monomer and low molecular weight oligomer (M/LMW) peptide accumulation. Cumulative evidence suggests that accumulation of M/LMW Aβ42 peptides occurs early, before high molecular weight oligomerization and plaque formation. Since synaptic alteration is the best pathologic correlate of cognitive dysfunction in AD, the spatial association of M/LMW Aβ peptide accumulation with pathology of MAP2 within neuronal processes and synaptic compartments early in the disease process reinforces the importance of intraneuronal Aβ accumulation in AD pathogenesis.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCA1 Region, HippocampalExtracellular SpaceGene ExpressionHumansMiceMice, TransgenicMicrotubule-Associated ProteinsNeuritesPeptide FragmentsProtein MultimerizationSynapsesSynaptic Transmissiontau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Mapt protein, mouseMicrotubule-Associated ProteinsMtap2 protein, mousePeptide Fragmentstau Proteins

Identifiers

PMID23372648
PMCPMC3553177
OpenAlexW2011738290

What OpenQuestion holds

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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.