Evidence map›Paper›PMID 41277110›Full record

ReviewAutophagy2026

Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.

Jiayi Lu, Damian N Di Florio, Patricia Boya, Sandra Maday, Wolfdieter Springer, Charleen T Chu

Abstract readReview
In one paragraph

Review in Autophagy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
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

6 authors.

Jiayi LuDepartment of Pathology/Division of Neuropathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0002-4276-3992
Damian N Di FlorioDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.ORCID 0000-0003-1619-5394
Patricia BoyaDepartment of Neuroscience and Movement Sciences, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0003-3045-951X
Sandra MadayDepartment of Neuroscience, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.ORCID 0000-0001-8664-4592
Wolfdieter SpringerDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.ORCID 0000-0002-1178-3149
Charleen T ChuDepartment of Pathology/Division of Neuropathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0002-5052-8271

Funding

Utilization of proteomics and lipidomics to identify modifiers of LBDU54NS110435 · NINDS · MAYO CLINIC JACKSONVILLE · PI DICKSON, DENNIS WILLIAM · 2019 to 2023
$14.5M
Regulation of Autophagy & Mitochondrial Recycling in Neuronal Cell Death- SupplementR01AG026389 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2007 to 2024
$6.0M
Training in the Neurobiology of Neurological DiseaseT32NS086749 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Omar El Gharbawie, REBECCA P SEAL · 2014 to 2026
$4.8M
Dendrite regulation by the mitochondrial kinase PINK1: Implications for PD/LBD Diversity SupplementR01NS101628 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Charleen T Chu, Zachary P Wills · 2017 to 2026
$4.0M
Molecular mechanisms of PINK1-PRKN directed mitochondrial quality controlRF1NS085070 · NINDS · MAYO CLINIC JACKSONVILLE · PI SPRINGER, WOLFDIETER · 2019 to 2019
$2.8M
Mitochondrial Sirtuin 3 in Parkinson's diseaseR01NS110085 · NINDS · MAYO CLINIC JACKSONVILLE · PI MCLEAN, PAMELA J, SPRINGER, WOLFDIETER · 2019 to 2023
$2.5M
Defining the roles and regulation of neuronal autophagyR01NS110716 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI MADAY, SANDRA L. · 2020 to 2024
$2.0M
Protein homeostasis in a frontotemporal dementia iPSC modelR21AG075814 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2022 to 2022
$435k
Astrocyte-neuron regulation of autophagy and lysosomal pathways in proteotoxic stress associated with alpha-synucleinopathiesR21AG088697 · NIA · UNIVERSITY OF PENNSYLVANIA · PI MADAY, SANDRA L. · 2024 to 2025
$434k
NIA NIH HHS R01 AG026389NIA NIH HHS R21 AG075814NIA NIH HHS R21 AG088697NINDS NIH HHS R01 NS101628NINDS NIH HHS R01 NS110085NINDS NIH HHS R01 NS110716NINDS NIH HHS RF1 NS085070NINDS NIH HHS T32 NS086749NINDS NIH HHS U54 NS110435
6 · The paper itself

Abstract

The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. Under normal conditions, macroautophagy/autophagy at the synapse plays a crucial role in synaptic pruning and plasticity, which occurs physiologically in the absence of disease- or aging-related stressors. Disruption of autophagy has profound effects on neuron development, structure, function, and survival. Neurons are dependent upon maintaining high-quality mitochondria, and alterations in selective mitochondrial autophagy (mitophagy) are heavily implicated in both genetic and environmental etiologies of neurodegenerative diseases. The unique spatial and functional demands of neurons result in differences in the regulation of metabolic, autophagic, mitophagic and biosynthetic processes compared to other cell types. Here, we review recent advances in autophagy and mitophagy research with an emphasis on studies involving primary neurons

Indexed as

AutophagyLearningMemoryMitophagyNervous System DiseasesSynapsesAnimalsHumansMitochondriaNeurodegenerative DiseasesNeuronsBiomarkersdementiadendritic spinesmitochondrianeurodegenerative diseasesneurodevelopmental disordersParkinson diseasesynaptic plasticity

Identifiers

PMID41277110
PMCPMC12758295

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.