Evidence map›Paper›PMID 26968346›Full record

ReviewTrends in neurosciences2016

The Autophagy-Lysosomal Pathway in Neurodegeneration: A TFEB Perspective.

Heidi Martini-Stoica, Yin Xu, Andrea Ballabio, Hui Zheng

Open access · greenAbstract readReview
In one paragraph

Review in Trends in neurosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
257citing papers in PubMed, 1 pooled it
24.1field-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

257 citing papers in PubMed, 1 synthesis or guideline pooled it, 417 citations in OpenAlex.

  1. Pooled it
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  19. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
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197 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

4 authors at 2 institutions in 2 countries.

Heidi Martini-StoicaHuffington Center on Aging, Baylor College of Medicine, Houston, TX, USA; Interdepartmental Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, TX, USA; Medical Scientist Training Program, Baylor College of Medicine, Houston, TX, USA.
Yin XuHuffington Center on Aging, Baylor College of Medicine, Houston, TX, USA.
Andrea BallabioDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX; Dan and Jan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX, USA; Telethon Institute of Genetics and Medicine (TIGEM) and Department of Translational Medical Sciences, Frederico II University, Naples, Italy.
Hui ZhengHuffington Center on Aging, Baylor College of Medicine, Houston, TX, USA; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX. Electronic address: huiz@bcm.edu.
Baylor College of Medicine · USTexas Children's Hospital · US

Funding

Knockin Mouse Models of Alzheimers DiseaseR01AG020670 · NIA · BAYLOR COLLEGE OF MEDICINE · PI Hui Zheng · 2002 to 2026
$9.1M
MODULATION OF CELLULAR CLEARANCE TO TREAT HUMAN DISEASER01NS078072 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI BALLABIO, ANDREA · 2012 to 2020
$3.1M
ROLE OF TFEB IN TAUOPATHYR01NS093652 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ZHENG, HUI · 2015 to 2025
$3.1M
Mechanism and therapy of AB-42-specific gamma-secretaseR01NS076117 · NINDS · SLOAN-KETTERING INST CAN RESEARCH · PI LI, YUEMING, ZHENG, HUI · 2011 to 2015
$2.8M
Knockin mouse models of Alzheimer's DiseaseRF1AG020670 · NIA · BAYLOR COLLEGE OF MEDICINE · PI ZHENG, HUI · 2022 to 2022
$2.3M
ROLE OF TFEB IN TAUOPATHYRF1NS093652 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ZHENG, HUI · 2021 to 2021
$1.5M
Extracellular Mechanisms of TFEB-mediated Clearance of pTau in TauopathiesF30AG050412 · NIA · BAYLOR COLLEGE OF MEDICINE · PI MARTINI-STOICA, HEIDI · 2015 to 2016
$84k
NIA NIH HHS F30 AG050412NIA NIH HHS R01 AG020670NIA NIH HHS RF1 AG020670NINDS NIH HHS R01 NS076117NINDS NIH HHS R01 NS078072NINDS NIH HHS R01 NS 078072-01A1NINDS NIH HHS R01 NS093652NINDS NIH HHS RF1 NS093652
6 · The paper itself

Abstract

The autophagy-lysosomal pathway (ALP) is involved in the degradation of long-lived proteins. Deficits in the ALP result in protein aggregation, the generation of toxic protein species, and accumulation of dysfunctional organelles, which are hallmarks of Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and prion disease. Decades of research have therefore focused on enhancing the ALP in neurodegenerative diseases. More recently, transcription factor EB (TFEB), a major regulator of autophagy and lysosomal biogenesis, has emerged as a leading factor in addressing disease pathology. We review the regulation of the ALP and TFEB and their impact on neurodegenerative diseases. We also offer our perspective on the complex role of autophagy and TFEB in disease pathogenesis and its therapeutic implications through the examination of prion disease.

Indexed as

AnimalsAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBrainHumansLysosomesNerve DegenerationNeurodegenerative DiseasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsTFEB protein, humanautophagy–lysosomal pathwayneurodegenerative diseaseprion diseaseTFEB

Identifiers

PMID26968346
PMCPMC4928589
OpenAlexW2293027573

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.