Evidence map›Paper›PMID 26240337›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

In vivo imaging of axonal transport of mitochondria in the diseased and aged mammalian CNS.

Yuji Takihara, Masaru Inatani, Kei Eto, Toshihiro Inoue, Alexander Kreymerman, Seiji Miyake, Shinji Ueno, Masatoshi Nagaya, Ayami Nakanishi, Keiichiro Iwao and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
7.7field-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

103 citing papers in PubMed, 171 citations in OpenAlex.

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  15. Astrocytes in the mouse brain respond bilaterally to unilateral retinal neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025
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43 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

18 authors at 7 institutions in 2 countries.

Yuji TakiharaDepartment of Ophthalmology, Faculty of Medical Science, University of Fukui, Fukui 910-1193, Japan; Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan;
Masaru InataniDepartment of Ophthalmology, Faculty of Medical Science, University of Fukui, Fukui 910-1193, Japan; Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan; inatani@u-fukui.ac.jp.
Kei EtoDivision of Homeostatic Development, Department of Developmental Physiology, National Institute for Physiological Sciences, Aichi 444-8585, Japan; Department of Physiological Sciences, SOKENDAI (The Graduate University for Advanced Studies), Aichi 444-8585, Japan;
Toshihiro InoueDepartment of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan;
Alexander KreymermanShiley Eye Institute, University of California, San Diego, La Jolla, CA 92093;
Seiji MiyakeDepartment of Ophthalmology, Faculty of Medical Science, University of Fukui, Fukui 910-1193, Japan;
Shinji UenoDepartment of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan;
Masatoshi NagayaDepartment of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan;
Ayami NakanishiDepartment of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan;
Keiichiro IwaoDepartment of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan;ORCID http://orcid.org/0000-0002-4102-9374
Yoshihiro TakamuraDepartment of Ophthalmology, Faculty of Medical Science, University of Fukui, Fukui 910-1193, Japan;
Hirotaka SakamotoUshimado Marine Institute, Graduate School of Natural Science and Technology, Okayama University, Okayama 701-4303, Japan;
Keita SatohUshimado Marine Institute, Graduate School of Natural Science and Technology, Okayama University, Okayama 701-4303, Japan;
Mineo KondoDepartment of Ophthalmology, Mie University Graduate School of Medicine, Mie 514-8507, Japan.
Tatsuya SakamotoUshimado Marine Institute, Graduate School of Natural Science and Technology, Okayama University, Okayama 701-4303, Japan;
Jeffrey L GoldbergShiley Eye Institute, University of California, San Diego, La Jolla, CA 92093;
Junichi NabekuraDivision of Homeostatic Development, Department of Developmental Physiology, National Institute for Physiological Sciences, Aichi 444-8585, Japan; Department of Physiological Sciences, SOKENDAI (The Graduate University for Advanced Studies), Aichi 444-8585, Japan;
Hidenobu TaniharaDepartment of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan;
University of Fukui · JPKumamoto University · JPNagoya University · JPOkayama University · JPThe Graduate University for Advanced Studies, SOKENDAI · JPUniversity of California San Diego · USMie University · JP

Funding

The role of mitochondrial fission/fusion in CNS axon regenerationF31NS087789 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KREYMERMAN, ALEXANDER · 2014 to 2016
$81k
NINDS NIH HHS F31 NS087789
6 · The paper itself

Abstract

The lack of intravital imaging of axonal transport of mitochondria in the mammalian CNS precludes characterization of the dynamics of axonal transport of mitochondria in the diseased and aged mammalian CNS. Glaucoma, the most common neurodegenerative eye disease, is characterized by axon degeneration and the death of retinal ganglion cells (RGCs) and by an age-related increase in incidence. RGC death is hypothesized to result from disturbances in axonal transport and in mitochondrial function. Here we report minimally invasive intravital multiphoton imaging of anesthetized mouse RGCs through the sclera that provides sequential time-lapse images of mitochondria transported in a single axon with submicrometer resolution. Unlike findings from explants, we show that the axonal transport of mitochondria is highly dynamic in the mammalian CNS in vivo under physiological conditions. Furthermore, in the early stage of glaucoma modeled in adult (4-mo-old) mice, the number of transported mitochondria decreases before RGC death, although transport does not shorten. However, with increasing age up to 23-25 mo, mitochondrial transport (duration, distance, and duty cycle) shortens. In axons, mitochondria-free regions increase and lengths of transported mitochondria decrease with aging, although totally organized transport patterns are preserved in old (23- to 25-mo-old) mice. Moreover, axonal transport of mitochondria is more vulnerable to glaucomatous insults in old mice than in adult mice. These mitochondrial changes with aging may underlie the age-related increase in glaucoma incidence. Our method is useful for characterizing the dynamics of axonal transport of mitochondria and may be applied to other submicrometer structures in the diseased and aged mammalian CNS in vivo.

Indexed as

AgingAnimalsAxonal TransportAxonsBiological TransportCentral Nervous SystemDisease Models, AnimalFemaleGlaucomaImaging, Three-DimensionalMaleMiceMice, Inbred BALB CMice, Inbred C57BLMitochondriaOptic Nerveagingin vivo imagingmammalian CNSmitochondrial axonal transportneurodegeneration

Identifiers

PMID26240337
PMCPMC4547257
OpenAlexW1934544298

What OpenQuestion holds

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Registered trials

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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.