Evidence map›Paper›PMID 29852219›Full record

ReviewNeurobiology of disease2019

TFEB dysregulation as a driver of autophagy dysfunction in neurodegenerative disease: Molecular mechanisms, cellular processes, and emerging therapeutic opportunities.

Constanza J Cortes, Albert R La Spada

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
12.2field-weighted citation impact, top 1% 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

110 citing papers in PubMed, 189 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
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  18. Article
  19. Review
  20. Article

50 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Constanza J CortesDepartments of Neurology, Neurobiology, and Cell Biology, Duke University School of Medicine, Durham, NC 27710, USA; Duke Center for Neurodegeneration & Neurotherapeutics, Duke University School of Medicine, Durham, NC 27710, USA.
Albert R La SpadaDepartments of Neurology, Neurobiology, and Cell Biology, Duke University School of Medicine, Durham, NC 27710, USA; Duke Center for Neurodegeneration & Neurotherapeutics, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: al.laspada@duke.edu.
Duke University · US

Funding

Molecular genetic regulation of autophagy in health and neurodegenerative diseaseR01AG033082 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LA SPADA, ALBERT R · 2009 to 2019
$4.0M
Enhanced skeletal muscle proteostasis as a determinant of CNS protein quality control and neural function in the aging brainRF1AG057264 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CORTES, CONSTANZA JAVIERA, LA SPADA, ALBERT R · 2017 to 2021
$2.7M
Deconstructing the cellular and molecular basis of SBMA motor neuron disease: From mechanism to therapyR01NS100023 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LA SPADA, ALBERT R · 2016 to 2020
$2.4M
Enhanced Skeletal Muscle Proteostasis as a Modulator of Alzheimer's DiseaseR03AG063215 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CORTES, CONSTANZA JAVIERA · 2019 to 2020
$309k
NIA NIH HHS R01 AG033082NIA NIH HHS R03 AG063215NIA NIH HHS RF1 AG057264NINDS NIH HHS R01 NS100023
6 · The paper itself

Abstract

Two decades ago, the recognition of protein misfolding and aggregate accumulation as defining features of neurodegenerative disease set the stage for a thorough examination of how protein quality control is maintained in neurons and in other non-neuronal cells in the central nervous system (CNS). Autophagy, a pathway of cellular self-digestion, has emerged as especially important for CNS proteostasis, and autophagy dysregulation has been documented as a defining feature of neurodegeneration in Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Transcription factor EB (TFEB) is one of the main transcriptional regulators of autophagy, as it promotes the expression of genes required for autophagosome formation, lysosome biogenesis, and lysosome function, and it is highly expressed in CNS. Over the last 7 years, TFEB has received considerable attention and TFEB dysfunction has been implicated in the pathogenesis of numerous neurodegenerative disorders. In this review, we delineate the current understanding of how TFEB dysregulation is involved in neurodegeneration, highlighting work done on AD, PD, HD, X-linked spinal & bulbar muscular atrophy, and amyotrophic lateral sclerosis. Because TFEB is a central node in defining autophagy activation status, efforts at understanding the basis for TFEB dysfunction are yielding insights into how TFEB might be targeted for therapeutic application, which may represent an exciting opportunity for the development of a treatment modality with broad application to neurodegeneration.

Indexed as

AnimalsAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsHumansNeurodegenerative DiseasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsAlzheimer's diseaseAmyotrophic lateral sclerosisAutophagyHuntington's diseaseLysosomeNeurodegenerationParkinson's diseasePolyglutamineSpinal & bulbar muscular atrophySynucleinopathyTranscription factor EB

Identifiers

PMID29852219
PMCPMC6291370
OpenAlexW2806423234

What OpenQuestion holds

Textmetadata
LicenceTDM
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.