Evidence map›Paper›PMID 31171723›Full record

ArticleThe Journal of biological chemistry2019

Tau isoform expression and phosphorylation in marmoset brains.

Govinda Sharma, Anni Huo, Taeko Kimura, Seiji Shiozawa, Reona Kobayashi, Naruhiko Sahara, Minaka Ishibashi, Shinsuke Ishigaki, Taro Saito, Kanae Ando and 5 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 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
2.1field-weighted citation impact, top 13% 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, 44 citations in OpenAlex.

  1. Article
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  7. Early molecular events of autosomal-dominant Alzheimer's disease in marmosets with PSEN1 mutations.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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  11. Review
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  18. Review
  19. Review
  20. A novel tau-based rhesus monkey model of Alzheimer's pathogenesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021
    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

15 authors at 5 institutions in 1 country.

Govinda SharmaLaboratory of Molecular Neuroscience, Faculty of Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Anni HuoLaboratory of Molecular Neuroscience, Faculty of Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Taeko KimuraLaboratory of Molecular Neuroscience, Faculty of Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Seiji ShiozawaDepartment of Physiology, School of Medicine, Keio University, Shinjuku, Tokyo, 160-8582, Japan.
Reona KobayashiDepartment of Physiology, School of Medicine, Keio University, Shinjuku, Tokyo, 160-8582, Japan.
Naruhiko SaharaDepartment of Functional Brain Imaging Research, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage, Chiba, Chiba 263-8555, Japan.
Minaka IshibashiResearch Division of Dementia and Neurodegenerative Disease, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Shinsuke IshigakiResearch Division of Dementia and Neurodegenerative Disease, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Taro SaitoLaboratory of Molecular Neuroscience, Faculty of Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Kanae AndoLaboratory of Molecular Neuroscience, Faculty of Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan.
Shigeo MurayamaTokyo Metropolitan Institute of Gerontology, Itabashi, Tokyo 173-0015, Japan.
Masato HasegawaTokyo Metropolitan Institute of Medical Science, Setagaya, Tokyo 156-8506, Japan.
Gen SobueResearch Division of Dementia and Neurodegenerative Disease, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Hideyuki OkanoDepartment of Physiology, School of Medicine, Keio University, Shinjuku, Tokyo, 160-8582, Japan.
Shin-Ichi HisanagaLaboratory of Molecular Neuroscience, Faculty of Sciences, Tokyo Metropolitan University, Minami-osawa, Hachioji, Tokyo 192-0397, Japan hisanaga-shinichi@tmu.ac.jp.ORCID 0000-0002-7572-472X
Tokyo Metropolitan University · JPKeio University · JPNagoya University · JPTokyo Metropolitan Institute of Medical Science · JPTokyo Metropolitan Institute of Gerontology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau is a microtubule-associated protein expressed in neuronal axons. Hyperphosphorylated tau is a major component of neurofibrillary tangles, a pathological hallmark of Alzheimer's disease (AD). Hyperphosphorylated tau aggregates are also found in many neurodegenerative diseases, collectively referred to as "tauopathies," and tau mutations are associated with familial frontotemporal lobar degeneration (FTLD). Previous studies have generated transgenic mice with mutant tau as tauopathy models, but nonhuman primates, which are more similar to humans, may be a better model to study tauopathies. For example, the common marmoset is poised as a nonhuman primate model for investigating the etiology of age-related neurodegenerative diseases. However, no biochemical studies of tau have been conducted in marmoset brains. Here, we investigated several important aspects of tau, including expression of different tau isoforms and its phosphorylation status, in the marmoset brain. We found that marmoset tau does not possess the "primate-unique motif" in its N-terminal domain. We also discovered that the tau isoform expression pattern in marmosets is more similar to that of mice than that of humans, with adult marmoset brains expressing only four-repeat tau isoforms as in adult mice but unlike in adult human brains. Of note, tau in brains of marmoset newborns was phosphorylated at several sites associated with AD pathology. However, in adult marmoset brains, much of this phosphorylation was lost, except for Ser-202 and Ser-404 phosphorylation. These results reveal key features of tau expression and phosphorylation in the marmoset brain, a potentially useful nonhuman primate model of neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAnimalsBrainCallithrixCells, CulturedDNA, ComplementaryHumansMiceMice, TransgenicPhosphorylationPhylogenyProtein Isoformstau ProteinsDNA, ComplementaryProtein Isoformstau Proteinsalternative splicingAlzheimer diseasedevelopmentFTLD-tauisoformmammalMAPTmarmosetneurodegenerationneurodegenerative diseasenon-human primatephosphorylationphylogeneticstau protein (tau)

Identifiers

PMID31171723
PMCPMC6663862
OpenAlexW2948483706

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.