Evidence map›Paper›PMID 29982981›Full record

ArticleMolecular neurobiology2019

Myostatin Is Associated With Cognitive Decline in an Animal Model of Alzheimer's Disease.

Yung-Shuen Lin, Fang-Yu Lin, Ya-Hsin Hsiao

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  14. Associations Between Circulating Levels of Myostatin and Plasma β-Amyloid 42/40 in a Biracial Cohort of Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023
    Article
  15. Article
  16. Review
  17. Early-stage Alzheimer's disease: are skeletal muscle and exercise the key?Journal of applied physiology (Bethesda, Md. : 1985) · 2023
    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

3 authors at 1 institution in 1 country.

Yung-Shuen LinDepartment of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Fang-Yu LinDepartment of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan.
Ya-Hsin HsiaoDepartment of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. yahsin@mail.ncku.edu.tw.ORCID http://orcid.org/0000-0003-2885-3905
National Cheng Kung University · TW

Funding

Ministry of Science and Technology, Taiwan MOST 105-2320-B-006-016 and MOST 106-2320-B-006-057-MY3
6 · The paper itself

Abstract

With aging, there are progressive functional declines in multiple organ systems. One of the major physiological problems observed in aged people is skeletal muscle loss. This age-related muscle loss causes muscle weakness and disability, which in turn might reduce the quality of life in older adults and lead to the progression of several diseases, particularly Alzheimer's disease (AD). Some researchers have hypothesized that loss of muscle mass and strength is linked to the risk of developing AD. In addition, unintended weight loss often occurs in AD patients and might reflect dementia severity. However, the causal relationship between muscle atrophy and cognitive deficits in AD is unclear. We found that double transgenic amyloid precursor protein and presenilin 1 (APP/PS1) mice that co-express APP and PS1 at older ages exhibited lower body weight and lean tissue mass than sex- and age-matched wild-type (WT) mice. In addition, muscle atrophy and the extent of memory decline were strongly correlated in APP/PS1 mice. Myostatin levels in the gastrocnemius (GAS) muscle of 12-month-old APP/PS1 mice were elevated. We determined that the cellular and molecular mechanism of muscle atrophy was through the ubiquitin-proteasome pathway. Furthermore, myostatin knockdown in the GAS muscles increased grip strength and muscle mass, leading to memory improvement in myostatin short-hairpin RNA-treated APP/PS1 mice. We conclude that high-level myostatin expression might mediate or trigger muscle atrophy and cognitive deficits.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBody CompositionCognitive DysfunctionConditioning, PsychologicalDisease Models, AnimalDisease ProgressionFearMiceMice, TransgenicMyostatinPresenilin-1Recognition, PsychologyAmyloid beta-Protein PrecursorMyostatinPresenilin-1Alzheimer’s diseaseAPP/PS1 transgenic miceMemory impairmentMyostatin

Identifiers

PMID29982981
OpenAlexW2825416037

What OpenQuestion holds

Textmetadata
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.