Evidence map›Paper›PMID 32009941›Full record

ArticleFrontiers in aging neuroscience2019

Aging Disrupts the Circadian Patterns of Protein Expression in the Murine Hippocampus.

Paula Adler, Cheng-Kang Chiang, Janice Mayne, Zhibin Ning, Xu Zhang, Bo Xu, Hai-Ying Mary Cheng, Daniel Figeys

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 40 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

8 authors at 3 institutions in 1 country.

Paula AdlerShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
Cheng-Kang ChiangShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
Janice MayneShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
Zhibin NingShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
Xu ZhangShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
Bo XuShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
Hai-Ying Mary ChengDepartment of Biology, University of Toronto Mississauga, Mississauga, ON, Canada.
Daniel FigeysShanghai Institute of Materia Medica-University of Ottawa Joint Research Centre on Systems and Personalized Pharmacology, University of Ottawa, Ottawa, ON, Canada.
University of Ottawa · CAJoint Research Center on Systems and Personalized PharmacologyUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is associated with cognitive decline and dysregulation of the circadian system, which modulates hippocampal-dependent memory as well as biological processes underlying hippocampal function. While circadian dysfunction and memory impairment are common features of aging and several neurodegenerative brain disorders, how aging impacts the circadian expression patterns of proteins involved in processes that underlie hippocampal-dependent memory is not well understood. In this study, we profiled the hippocampal proteomes of young and middle-aged mice across two circadian cycles using quantitative mass spectrometry in order to explore aging-associated changes in the temporal orchestration of biological pathways. Of the ∼1,420 proteins that were accurately quantified, 15% (214 proteins) displayed circadian rhythms in abundance in the hippocampus of young mice, while only 1.6% (23 proteins) were rhythmic in middle-aged mice. Remarkably, aging disrupted the circadian regulation of proteins involved in cellular functions critical for hippocampal function and memory, including dozens of proteins participating in pathways of energy metabolism, neurotransmission, and synaptic plasticity. These included processes such as glycolysis, the tricarboxylic acid cycle, synaptic vesicle cycling, long-term potentiation, and cytoskeletal organization. Moreover, aging altered the daily expression rhythms of proteins implicated in hallmarks of aging and the pathogenesis of several age-related neurodegenerative brain disorders affecting the hippocampus. Notably, we identified age-related alterations in the rhythmicity of proteins involved in mitochondrial dysfunction and loss of proteostasis, as well as proteins involved in the pathogenesis of disorders such as Alzheimer's disease and Parkinson's disease. These insights into aging-induced changes in the hippocampal proteome provide a framework for understanding how the age-dependent circadian decline may contribute to cognitive impairment and the development of neurodegenerative diseases during aging.

Indexed as

agingcircadianhippocampusmass spectrometryneurodegenerative diseasesproteomics

Identifiers

PMID32009941
PMCPMC6974521
OpenAlexW2999906582

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.