Evidence map›Paper›PMID 31542152›Full record

ReviewBiological psychiatry2020

Neuronal Autophagy in Synaptic Functions and Psychiatric Disorders.

Toshifumi Tomoda, Kun Yang, Akira Sawa

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

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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.

Toshifumi TomodaCentre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada. Electronic address: ttomoda1@gmail.com.
Kun YangDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Akira SawaDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; Department of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. Electronic address: asawa1@jhmi.edu.

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
WOUND MIGRATION FORCE MONITORINGP41RR001192 · NCRR · UNIVERSITY OF CALIFORNIA-IRVINE · PI CHOI, BERNARD · 1985 to 2011
$14.2M
High throughput marker for cognitive deficit: cellular autofluorescenceR01MH107730 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2018 to 2022
$3.0M
DISC1-dependent defects in neural fate, corticogenesis and cognition in psychosisR01MH105660 · NIMH · JOHNS HOPKINS UNIVERSITY · PI ISHIZUKA, KOKO, SAWA, AKIRA · 2014 to 2018
$2.8M
Oxidative stress and schizophrenia: combination of cell biology and brain imagingR01MH092443 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2015
$1.8M
NCRR NIH HHS P41 RR001192NIMH NIH HHS P50 MH094268NIMH NIH HHS R01 MH092443NIMH NIH HHS R01 MH105660NIMH NIH HHS R01 MH107730
6 · The paper itself

Abstract

Homeostatic maintenance of physiological functions is fundamental to organismal well-being. Disruption or imbalance in homeostasis results in functional disturbances at molecular, cellular, and tissue levels, leading to manifestation as physical and mental illnesses. Homeostatic imbalance is caused by a range of pathophysiological mechanisms, including disrupted reduction-oxidation reactions, inflammatory responses, metabolic disturbances, or failure in quality control of cellular proteins and organelles. However, the roles for the protein/organelle quality control in the regulation of behaviors, in particular of cognitive processes, had not been well documented, until recent reports finally supported this concept. The frontline studies in neuroscience have revealed that synaptic components (e.g., synaptic proteins, organelles, neurotransmitters and their receptors) are selectively degraded by autophagy, a cellular recycling machinery implicated in surveillance and quality control of proteins and organelles responsible for the maintenance of cellular homeostasis. Apart from the canonical role of autophagy in supporting cell viability, synaptic autophagy appears to regulate synapse remodeling and plasticity. Consistently, emerging evidence suggests novel roles of autophagy in memory encoding, information processing, or cognitive functions. In this review, we overview recent progress in understanding the roles of neuronal autophagy in homeostatic maintenance of synaptic functions, with particular focus on how disruptions in these processes may contribute to the pathophysiology of psychiatric disorders.

Indexed as

AutophagyMental DisordersHomeostasisHumansNeuronal PlasticityNeuronsAggregateAutophagyCognitionHomeostasisPsychiatric disordersSynapse

Identifiers

PMID31542152
PMCPMC6986983

What OpenQuestion holds

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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.