Evidence map›Paper›PMID 29439348›Full record

ArticleJournal of Alzheimer's disease : JAD2018

Evolvability of Amyloidogenic Proteins in Human Brain.

Makoto Hashimoto, Gilbert Ho, Shuei Sugama, Yoshiki Takamatsu, Yuka Shimizu, Takato Takenouchi, Masaaki Waragai, Eliezer Masliah

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Cancer Cells Enter an Adaptive Persistence to Survive Radiotherapy and Repopulate Tumor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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  7. Therapeutic Potential ofParkinson's disease · 2021
    Review
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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

8 authors at 4 institutions in 2 countries.

Makoto HashimotoTokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Gilbert HoPCND Neuroscience Research Institute, Poway, CA, USA.
Shuei SugamaDepartment of Physiology, Nippon Medical School, Tokyo, Japan.
Yoshiki TakamatsuTokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Yuka ShimizuTokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Takato TakenouchiInstitute of Agrobiological Sciences, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan.
Masaaki WaragaiTokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Eliezer MasliahDivision of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Tokyo Metropolitan Institute of Medical Science · JPNational Agriculture and Food Research Organization · JPNational Institutes of Health · USNippon Medical School · JP

Funding

Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
6 · The paper itself

Abstract

Currently, the physiological roles of amyloidogenic proteins (APs) in human brain, such as amyloid-β and α-synuclein, are elusive. Given that many APs arose by gene duplication and have been resistant against the pressures of natural selection, APs may be associated with some functions that are advantageous for survival of offspring. Nonetheless, evolvability is the sole physiological quality of APs that has been characterized in microorganisms such as yeast. Since yeast and human brain may share similar strategies in coping with diverse range of critical environmental stresses, the objective of this paper was to discuss the potential role of evolvability of APs in aging-associated neurodegenerative disorders, including Alzheimer's disease and Parkinson's disease. Given the heterogeneity of APs in terms of structure and cytotoxicity, it is argued that APs might be involved in preconditioning against diverse stresses in human brain. It is further speculated that these stress-related APs, most likely protofibrillar forms, might be transmitted to offspring via the germline, conferring preconditioning against forthcoming stresses. Thus, APs might represent a vehicle for the inheritance of the acquired characteristics against environmental stresses. Curiously, such a characteristic of APs is reminiscent of Charles Darwin's 'gemmules', imagined molecules of heritability described in his pangenesis theory. We propose that evolvability might be a physiological function of APs during the reproductive stage and neurodegenerative diseases could be a by-product effect manifested later in aging. Collectively, our evolvability hypothesis may play a complementary role in the pathophysiology of APs with the conventional amyloid cascade hypothesis.

Indexed as

Evolution, MolecularAmyloidogenic ProteinsAnimalsBrainHumansModels, BiologicalAmyloidogenic ProteinsAlzheimer’s diseaseamyloidogenic proteinscancersevolvabilityneurodegenerative diseasestresstransmissionyeast prionγ-synuclein

Identifiers

PMID29439348
PMCPMC5817905
OpenAlexW2785869293

What OpenQuestion holds

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LicenceCC BY-NC
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.