Evidence map›Paper›PMID 30741673›Full record

ReviewJournal of Alzheimer's disease : JAD2019

Transgenerational Interaction of Alzheimer's Disease with Schizophrenia through Amyloid Evolvability.

Yoshiki Takamatsu, Gilbert Ho, Masaaki Waragai, Ryoko Wada, Shuei Sugama, Takato Takenouchi, Eliezer Masliah, Makoto Hashimoto

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Therapeutic Potential ofParkinson's disease · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. 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

8 authors at 4 institutions in 2 countries.

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

Alzheimer's disease (AD), the most common neurodegenerative dementia, leads to memory dysfunction due to widespread neuronal loss associated with aggregation of amyloidogenic proteins (APs), while schizophrenia (SCZ) represents a major psychiatric disorder characterized by delusions, hallucinations, and other cognitive abnormalities, the underlying mechanisms of which remain obscure. Although AD and SCZ partially overlap in terms of psychiatric symptoms and some aspects of cognitive impairment, the causal relationship between AD and SCZ is unclear. Based on the similarity of APs with yeast prion in terms of stress-induced protein aggregation, we recently proposed that evolvability of APs might be an epigenetic phenomenon to transmit stress information of parental brain to cope with the stressors in offspring. Although amyloid evolvability may be beneficial in evolution, AD might be manifested during parental aging as the mechanism of antagonistic pleiotropy phenomenon. Provided that accumulating evidence implicates stress as an important factor in SCZ, the main objective of this paper is to better understand the possible connection of AD and SCZ through amyloid evolvability. Hypothetically, the delivery of information of stress by APs may be less efficient under the decreased evolvability conditions such as disease-modifying treatment, leading to SCZ in offspring. Conversely, the increased evolvability conditions including gene mutations of APs are supposed to be beneficial for offspring, but might lead to AD in parents. Collectively, AD and SCZ might transgenerationally interfere with each other through amyloid evolvability, and this could explain why both AD and SCZ have not been selected out through evolution.

Indexed as

Alzheimer DiseaseAmyloidogenic ProteinsAnimalsBrainHumansSchizophreniaAmyloidogenic ProteinsAlzheimer’s diseaseamyloid-βantagonistic pleiotropydisease-modifying therapyevolvabilitynatural selectionschizophreniatransgenerational

Identifiers

PMID30741673
PMCPMC6484278
OpenAlexW2912333635

What OpenQuestion holds

Textmetadata
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.