Evidence map›Paper›PMID 30358161›Full record

ArticleBrain and behavior2018

Association of deposition of tau and amyloid-β proteins with structural connectivity changes in cognitively normal older adults and Alzheimer's disease spectrum patients.

Yoko Shigemoto, Daichi Sone, Norihide Maikusa, Nobuyuki Okamura, Shozo Furumoto, Yukitsuka Kudo, Masayo Ogawa, Harumasa Takano, Yuma Yokoi, Masuhiro Sakata and 4 more

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 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

14 authors at 2 institutions in 1 country.

Yoko ShigemotoIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.ORCID 0000-0003-2524-2498
Daichi SoneIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
Norihide MaikusaIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
Nobuyuki OkamuraDivision of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
Shozo FurumotoDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai, Japan.
Yukitsuka KudoDepartment of Geriatric and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Masayo OgawaIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
Harumasa TakanoIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
Yuma YokoiDepartment of Psychiatry, National Center of Neurology and Psychiatry, Tokyo, Japan.
Masuhiro SakataDepartment of Psychiatry, National Center of Neurology and Psychiatry, Tokyo, Japan.
Tadashi TsukamotoDepartment of Neurology, National Center of Neurology and Psychiatry, Tokyo, Japan.
Koichi KatoIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
Noriko SatoDepartment of Radiology, National Center of Neurology and Psychiatry, Tokyo, Japan.
Hiroshi MatsudaIntegrative Brain Imaging Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
National Center of Neurology and Psychiatry · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlzheimer's disease (AD) is characterized by accumulation of extracellular amyloid-β and intracellular tau neurofibrillary tangles. The recent advent of tau positron emission tomography (PET) has enabled in vivo assessment of tau pathology. The aim of this study was to explore whether tau deposition influences the structural connectivity in amyloid-negative and amyloid-positive groups, and further explore the difference between the groups.

methodsWe investigated 18 patients with amnestic mild cognitive impairment/mild AD (AD-spectrum group) and 35 cognitively normal older adults (CN group) using diffusion MRI, amyloid, and tau PET imaging. Diffusion connectometry was performed to identify white matter pathways correlated with each of the six variables of tau deposition in the bilateral hippocampi, temporal lobes, posterior and anterior cingulate cortices, precunei, orbitofrontal lobes, and entire cerebrum.

resultsThe CN group showed increased connectivity along with an increased tau deposition in the bilateral hippocampi, temporal lobes, and entire cerebrum, whereas the AD-spectrum group showed decreased connectivity in the bilateral hippocampi, temporal lobes, anterior and posterior cingulate cortices, precunei, and entire cerebrum.

conclusionThese findings suggest that tau deposition in the CN group seems to induce a compensatory response against early neuronal injury or chronic inflammation associated with normal aging, whereas the coexistence of amyloid and tau in the AD-spectrum group seems to outweigh the compensatory response leading to decreased connectivity, suggesting that amyloid plays a crucial role in alternating structural connectivity.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesBrainCognitionCognitive DysfunctionFemaleHumansMaleNeural PathwaysPositron-Emission Tomographytau ProteinsWhite MatterAmyloid beta-Peptidestau ProteinsAlzheimer’s diseasediffusion tensor imagingstructural networktau PET

Identifiers

PMID30358161
PMCPMC6305935
OpenAlexW2898242226

What OpenQuestion holds

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LicenceCC BY
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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.