Evidence map›Paper›PMID 26461913›Full record

ArticlePloS one2015

Longitudinal Assessment of Tau Pathology in Patients with Alzheimer's Disease Using [18F]THK-5117 Positron Emission Tomography.

Aiko Ishiki, Nobuyuki Okamura, Katsutoshi Furukawa, Shozo Furumoto, Ryuichi Harada, Naoki Tomita, Kotaro Hiraoka, Shoichi Watanuki, Yoichi Ishikawa, Tetsuro Tago and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Longitudinal Assessment of Tau-Associated Pathology byDiagnostics (Basel, Switzerland) · 2021
    Article
  8. Article
  9. A multicenter comparison of [European journal of nuclear medicine and molecular imaging · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Neuroimaging in aging and neurologic diseases.Handbook of clinical neurology · 2019
    Review
  18. Effective Diagnosis of Alzheimer's DiseaseFrontiers in genetics · 2019
    Article
  19. Article
  20. Evaluation ofJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2018
    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

16 authors at 1 institution in 1 country.

Aiko IshikiDepartment of Geriatrics and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Nobuyuki OkamuraDepartment of Pharmacology, Tohoku University School of Medicine, Sendai city, Miyagi prefecture, Japan; Division of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Katsutoshi FurukawaDepartment of Geriatrics and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Shozo FurumotoDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Ryuichi HaradaDivision of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Naoki TomitaDepartment of Geriatrics and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Kotaro HiraokaDivision of Cyclotron Nuclear Medicine, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Shoichi WatanukiDivision of Cyclotron Nuclear Medicine, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Yoichi IshikawaDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Tetsuro TagoDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Yoshihito FunakiDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Ren IwataDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Manabu TashiroDivision of Cyclotron Nuclear Medicine, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Kazuhiko YanaiDepartment of Pharmacology, Tohoku University School of Medicine, Sendai city, Miyagi prefecture, Japan.
Yukitsuka KudoDivision of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan; Division of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Hiroyuki AraiDepartment of Geriatrics and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, Sendai city, Miyagi prefecture, Japan.
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The formation of neurofibrillary tangles is believed to contribute to the neurodegeneration observed in Alzheimer's disease (AD). Postmortem studies have shown strong associations between the neurofibrillary pathology and both neuronal loss and the severity of cognitive impairment. However, the temporal changes in the neurofibrillary pathology and its association with the progression of the disease are not well understood. Tau positron emission tomography (PET) imaging is expected to be useful for the longitudinal assessment of neurofibrillary pathology in the living brain. Here, we performed a longitudinal PET study using the tau-selective PET tracer [18F]THK-5117 in patients with AD and in healthy control subjects. Annual changes in [18F]THK-5117 binding were significantly elevated in the middle and inferior temporal gyri and in the fusiform gyrus of patients with AD. Compared to patients with mild AD, patients with moderate AD showed greater changes in the tau load that were more widely distributed across the cortical regions. Furthermore, a significant correlation was observed between the annual changes in cognitive decline and regional [18F]THK-5117 binding. These results suggest that the cognitive decline observed in patients with AD is attributable to the progression of neurofibrillary pathology. Longitudinal assessment of tau pathology will contribute to the assessment of disease progression and treatment efficacy.

Indexed as

Aniline CompoundsPositron-Emission TomographyQuinolinesAgedAged, 80 and overAlzheimer DiseaseCase-Control StudiesDemographyFemaleHumansLongitudinal StudiesMaletau Proteins6-((3-fluoro-2-hydroxy)propoxy)-2-(4-methylaminophenyl)quinolineAniline CompoundsQuinolinestau Proteins

Identifiers

PMID26461913
PMCPMC4604169
OpenAlexW2341630503

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.