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The Autophagy–Lysosomal Pathway in Neurodegeneration: A TFEB Perspective
Open accessAbstract
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.
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“TFE3 or TFEB upregulation or activation through pharmacological inhibition of mTORC1 can trigger clearance of excess α-synuclein and halt the progression of neurotoxicity17–22.”
From PDCD4 triggers α-synuclein accumulation and motor deficits via co-suppressing TFE3 and TFEB translation in a model of Parkinson’s disease (2024) · cites this paper as [20]
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“Molecular and histopathologic analyses of patient tissues demonstrate mislocalized or accumulated autophagy machinery, pathogenic mutations underlying familial neurodegenerative diseases disable known autophagy-related factors, and genetically ablating autophagy effectors produce neurodegeneration in cell and animal model systems [74–81], supporting a role for autophagy dysfunction in the devel”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [79]
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BackgroundInfluentialLysosome regulation of microglia in Alzheimer’s disease via TFEB–vacuolar ATPase
(2023) · Nature Neuroscience · doi:10.1038/s41593-023-01495-1 · Cited by 8
Brunialti, E., Rizzi, N., Pinto‐Costa, R., Villa, A. M., Panzeri, A., Meda, C., Rebecchi, M., Monte, D. A. D., & Ciana, P. (2024) · Autophagy · doi:10.1080/15548627.2024.2334111 · Cited by 9
“…chosen to analyze the tdTomato reporter in different brain areas where cellular complexity is the most relevant obstacle to the development of functional drugs acting through a ubiquitous target like TFEB, which is involved in a number of homeostatic processes in different areas of the brain [70].”
BackgroundLiu, Y., Liu, Q., Shang, H., Li, J., Chai, H., Wang, K., Guo, Z., Luo, T., Liu, S., Liu, Y., et al. (2024) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2024.108721 · Cited by 9
Chen, B., Liu, Y., Luo, S., Zhou, J., Wang, Y., He, Q., Zhuang, G., Hu, H., Ma, F., Xiao, X., et al. (2024) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2024.11.035 · Cited by 9
Wang, Z., Zhang, L., Wu, T., Xu, P., Li, L., Yang, X., Zhang, M., Liu, Y., & Liu, Y. (2025) · British Journal of Pharmacology · doi:10.1111/bph.17378 · Cited by 10
“…protein aggregation, the production of toxic protein species, and the accumulation of dysfunctional organelles, which are characteristic features of neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease and others (Martini-Stoica et al., 2016; W. Zhang et al., 2022).”
Phase-separated Condensates in Autophagosome Formation and Autophagy Regulation
Wang, Z., & Zhang, H. (2025) · Journal of Molecular Biology · doi:10.1016/j.jmb.2025.168964 · Cited by 9
Nobiletin‐mediated autophagy mitigates nanoplastic‐induced toxicity in human intestinal Caco‐2 cells
Yu, J., Yoon, J., Park, M., & Lee, H. (2025) · The FASEB Journal · doi:10.1096/fj.202402761r · Cited by 9
“13 Nobiletin (NOB), a citrus peel flavonoid with notable anti-inflammatory and antioxidant properties, has been studied for its role in activating autophagy.”
An Emerging Role for Phosphoinositides in the Pathophysiology of Parkinson’s Disease
Schechter, M., & Sharon, R. (2021) · Journal of Parkinson s Disease · doi:10.3233/jpd-212684 · Cited by 11
“A role for the retromer in SV recycling, autophagy and lysosomal degradation has been reported [250, 251].”
BackgroundCell Biology of Parkin: Clues to the Development of New Therapeutics for Parkinson’s Disease
Patel, J., Panicker, N., Dawson, V. L., & Dawson, T. M. (2022) · CNS Drugs · doi:10.1007/s40263-022-00973-7 · Cited by 9
Pang, P., Zhang, X., Yuan, J., Yan, H., & Yan, D. (2023) · Food and Chemical Toxicology · doi:10.1016/j.fct.2023.113818 · Cited by 9
Transcription Factor EB: A Promising Therapeutic Target for Ischemic Stroke
Shao, J., Lang, Y., Ding, M., Yin, X. L., & Cui, L. (2023) · Current Neuropharmacology · doi:10.2174/1570159x21666230724095558 · Cited by 9
“TFEB has confirmed positive effects on neurodegenerative diseases [16], tumors [17], and kidney-related diseases [18]; however, its effects on AIS remain unclear.”
BackgroundChen, K., Padilla, C. G., Kiselyov, K. I., & Kozai, T. D. Y. (2023) · Biomaterials · doi:10.1016/j.biomaterials.2023.122316 · Cited by 9
A splicing variant of TFEB negatively regulates the TFEB-autophagy pathway
Park, J.-Y., Sohn, H., Koh, Y. H., & Jo, C. (2021) · Scientific Reports · doi:10.1038/s41598-021-00613-y · Cited by 9
Investigation of ATG16L1 rs2241880 Polymorphism with Cancer Risk: A Meta-Analysis
Moazeni‐Roodi, A., Tabasi, F., Ghavami, S., & Hashemi, M. M. (2019) · Medicina · doi:10.3390/medicina55080425 · Cited by 9
A Preview of Selected Articles
Atkinson, S. P. (2017) · Stem Cells · doi:10.1002/stem.2745 · Cited by 9
Cao, B., Chen, X., Li, Y., Zhou, T., Chen, N., Guo, Y., Zhao, M., Guo, C., Shi, Y., Wang, Q., et al. (2024) · npj Parkinson's Disease · doi:10.1038/s41531-024-00760-9 · Cited by 8
Song, J., Wang, T., Hong, J., Wang, Y., & Feng, J. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.111630 · Cited by 8
Autophagy in the pharmacological activities of celastrol (Review)
Zhang, C., Wang, W., Du, C., Li, H., Zhou, K., Luan, Z., Chang, Y., Liu, S., & Wei, Y. (2023) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2023.11967 · Cited by 7
“TFEB, the tran‐ scription factor that binds to a promoter motif coordinating the transcription of multiple autophagic and lysosomal genes, is known as the key regulator of the autophagy pathway (76).”
BackgroundHLH-30/TFEB modulates autophagy to improve proteostasis in Aβ transgenic Caenorhabditis elegans
Lin, H., Zhang, C., Gao, Y., Zhou, Y., Ma, B., Jiang, J., Long, X., Yimamu, N., Zhong, K., Li, Y., et al. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1433030 · Cited by 8
Zhou, D., Yan, H., Yang, S., Zhang, Y., Xu, X., Cen, X., Lei, K., & Xia, H. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.741219 · Cited by 8
“SC75741 Activates TFEB Independently of mTORC1 Activity TFEB, transcription factor EB, which positively regulates the expression autophagy-related genes to induce autophagosome formation, autophagosome-lysosome fusion, and degradation of autophagy substrates (Martini-Stoica et al., 2016).”
BackgroundPopp, L., Gomez, E. J., Orji, W. U., Ho, M., Suh, J., & Segatori, L. (2017) · Virology · doi:10.1016/j.virol.2017.06.030 · Cited by 8
“Finally, the autophagy-inducing properties of AAV could be harnessed to enhance autophagic clearance for the treatment of diseases characterized by deficient autophagy, which results in accumulation of proteinaceous aggregates and dysfunctional organelles (Martini-Stoica et al., 2016).”
BackgroundA Therapeutic Target for Inhibition of Neurodegeneration: Autophagy
Pupyshev, A. B., Короленко, Т. А., & Tikhonova, M. A. (2017) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-017-0519-7 · Cited by 8
“Transcription factor EB (TFEB) is of great interest; this regulates both lysosome biogenesis and the formation of autophagosomes, activating both vesicle fl ows [Settembre et al., 2011; Martini-Stoica et al., 2016].”
Krohn, L., Heilbron, K., Blauwendraat, C., Reynolds, R. H., Yu, E., Senkevich, K. A., Rudakou, U., Estiar, M. A., Gustavsson, E. K., Brolin, K. A., et al. (2021) · medRxiv · doi:10.1101/2021.09.08.21254232 · Cited by 8
Ahnaou, A., & Drinkenburg, W. H. I. M. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104897 · Cited by 7
TFEB overexpression alleviates autophagy-lysosomal deficits caused by progranulin insufficiency
Nader, W. O., Brown, K. S., Boyle, N. R., Kaplelach, A. K., Abdelaziz, S. M., Davis, S. E., Aljabi, Q., Hakim, A. R., Davidson, A. G., Vollmer, G. A., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-12268-0 · Cited by 9
“TFEB’s activation of lysosomal biogenesis and stimulation of autophagy may mediate its protective effects against neurodegenerative pathology 71,72 .”
Liu, S., Bu, Q., Tong, J., Wang, Z., Cui, J., Cao, H., Ma, H., Cao, B., An, X., & Song, Y. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24108751 · Cited by 7
Protein modification regulated autophagy in Bombyx mori and Drosophila melanogaster
Wu, W., Lin, L., Zhao, Y., Li, H., & Zhang, R. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1281555 · Cited by 7
“While Beclin 1/Atg5 is known to regulate autophagy associated with learning and memory in rats (Xu et al., 2016; Wang et al., 2021a), how do Atgs in fl uence learning and memory in insects?”
Melanin deposition and key molecular features in Xenopus tropicalis oocytes
Yi, H., Hang, J., Shen, J., Yang, S., Liu, H., Deng, J., Han, S., Feng, X., Chen, Y., Liang, W., et al. (2025) · BMC Biology · doi:10.1186/s12915-025-02168-0 · Cited by 7
Kraut, R. S., & Knust, E. (2019) · PLoS ONE · doi:10.1371/journal.pone.0220220 · Cited by 7
“Many of these genes encode proteins involved in trafficking, which is not surprising, given the high membrane turnover observed in photoreceptors required to maintain homeostasis [54–57].”
BackgroundRosario-Rodríguez, L. J., Colón, K., Borges-Vélez, G., Negrón, K., & Meléndez, L. M. (2018) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-018-9794-5 · Cited by 7
Metadata
- Authors
- Martini-Stoica, H., Xu, Y., Ballabio, A., & Zheng, H.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Zheng, Hui
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2016-04
- Volume
- 39
- Issue
- 4
- Pages
- 221-234
- ISSN
- 0166-2236 (ISSN-L)
- PMC
- PMC4928589
- OpenAlex
- W2293027573
- Cited by
- 436
- References
- 127
- Citations by year
- 2026: 38 · 2025: 41 · 2024: 46 · 2023: 65 · 2022: 48 · 2021: 53 · 2020: 43 · 2019: 34 · 2018: 27 · 2017: 31 · 2016: 10
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (RF1AG020670, F30AG050412, R01AG020670)
- National Institute of Neurological Disorders and Stroke (R01NS076117, RF1NS093652, R01NS078072, R01NS093652)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- autophagy-lysosome pathway, TFEB, neurodegenerative diseases, lysosomal biogenesis, protein aggregation, Alzheimer's disease, Parkinson's disease, Huntington's disease, prion disease, autophagy regulation, therapeutic target
- MeSH terms
- Animals, Autophagy, Brain, Humans, Lysosomes, Nerve Degeneration, Neurodegenerative Diseases, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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