The dual and emerging role of physical exercise-induced TFEB activation in the protection against Alzheimer's disease.

التفاصيل البيبلوغرافية
العنوان:	The dual and emerging role of physical exercise-induced TFEB activation in the protection against Alzheimer's disease.
المؤلفون:	Morais GP; Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil., de Sousa Neto IV; School of Physical Education and Sport of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil., Marafon BB; Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil., Ropelle ER; Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, São Paulo, Brazil., Cintra DE; Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, São Paulo, Brazil.; Nutrigenomics and Lipids Research Center, CELN, School of Applied Sciences, UNICAMP, São Paulo, São Paulo, Brazil., Pauli JR; Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, São Paulo, Brazil., Silva ASRD; Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.; School of Physical Education and Sport of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
المصدر:	Journal of cellular physiology [J Cell Physiol] 2023 May; Vol. 238 (5), pp. 954-965. Date of Electronic Publication: 2023 Apr 03.
نوع المنشور:	Journal Article; Research Support, Non-U.S. Gov't; Review
اللغة:	English
بيانات الدورية:	Publisher: Wiley-Liss Country of Publication: United States NLM ID: 0050222 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4652 (Electronic) Linking ISSN: 00219541 NLM ISO Abbreviation: J Cell Physiol Subsets: MEDLINE
أسماء مطبوعة:	Publication: New York, NY : Wiley-Liss Original Publication: Philadelphia, Wistar Institute of Anatomy and Biology.
مواضيع طبية MeSH:	Alzheimer Disease/therapy , Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics , Basic Helix-Loop-Helix Leucine Zipper Transcription Factors*/metabolism, Animals ; Amyloid beta-Peptides/metabolism ; Autophagy ; Exercise ; Lysosomes/metabolism ; Muscle, Skeletal/metabolism
مستخلص:	The mechanisms of autophagy have been related to Alzheimer's disease (AD) pathogenesis by the endosomal-lysosomal system, having a critical function in forming amyloid-β (Aβ) plaques. Nevertheless, the exact mechanisms mediating disease pathogenesis remain unclear. The transcription factor EB (TFEB), a primary transcriptional autophagy regulator, improves gene expression, mediating lysosome function, autophagic flux, and autophagosome biogenesis. In this review, we present for the first time the hypothesis of how TFEB, autophagy, and mitochondrial function are interconnected in AD, providing a logical foundation for unraveling the critical role of chronic physical exercise in this process. Aerobic exercise training promotes Adiponectin Receptor 1 (AdipoR1)/AMP-activated protein kinase (AMPK)/TFEB axis activation in the brain of the AD animal model, which contributes to alleviated Aβ deposition and neuronal apoptosis while improving cognitive function. Moreover, TFEB upregulates Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and nuclear factor erythroid 2-related factor 2 (NRF-2), improving mitochondrial biogenesis and redox status. In addition, tissue contraction activates calcineurin in skeletal muscle, which induces TFEB nuclear translocation, raising the hypothesis that the same would occur in the brain. Thus, a deep and comprehensive exploration of the TFEB could provide new directions and strategies for preventing AD. We conclude that chronic exercise can be an effective TFEB activator, inducing autophagy and mitochondrial biogenesis, representing a potential nonpharmacological strategy contributing to brain health. (© 2023 Wiley Periodicals LLC.)
References:	Bao, J., Zheng, L., Zhang, Q., Li, X., Zhang, X., Li, Z., Bai, X., Zhang, Z., Huo, W., Zhao, X., Shang, S., Wang, Q., Zhang, C., & Ji, J. (2016). Deacetylation of TFEB promotes fibrillar Aβ degradation by upregulating lysosomal biogenesis in microglia. Protein & Cell, 7(6), 417-433. Bateman, R. J., Munsell, L. Y., Morris, J. C., Swarm, R., Yarasheski, K. E., & Holtzman, D. M. (2006). Human amyloid-β synthesis and clearance rates as measured in cerebrospinal fluid in vivo. Nature Medicine, 12(7), 856-861. Bernardo, T. C., Marques-Aleixo, I., Beleza, J., Oliveira, P. J., Ascensão, A., & Magalhães, J. (2016). Physical exercise and brain mitochondrial fitness: The possible role against Alzheimer's disease: Exercise and Alzheimer's disease. Brain Pathology, 26(5), 648-663. Boland, B., & Platt, F. M. (2015). Bridging the age spectrum of neurodegenerative storage diseases. Best Practice & Research Clinical Endocrinology & Metabolism, 29(2), 127-143. Butterfield, D. A., & Boyd-Kimball, D. (2004). Amyloid β-peptide (1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain. Brain Pathology, 14(4), 426-432. C Reese, L., & Taglialatela, G. (2011). A role for calcineurin in Alzheimer's disease. Current Neuropharmacology, 9(4), 685-692. Caccamo, A., Majumder, S., Richardson, A., Strong, R., & Oddo, S. (2010). Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-β, and Tau. Journal of Biological Chemistry, 285(17), 13107-13120. Chen, H., & Chan, D. C. (2006). Critical dependence of neurons on mitochondrial dynamics. Current Opinion in Cell Biology, 18(4), 453-459. Choi, D. H., Kwon, I. S., Koo, J. H., Jang, Y. C., Kang, E. B., Byun, J. E., Um, H. S., Park, H. S., Yeom, D. C., Cho, I. H., & Cho, J. Y. (2014). The effect of treadmill exercise on inflammatory responses in rat model of streptozotocin-induced experimental dementia of Alzheimer's type. Journal of Exercise Nutrition and Biochemistry, 18(2), 225-233. https://doi.org/10.5717/jenb.2014.18.2.225. de la Cueva, M., Antequera, D., Ordoñez-Gutierrez, L., Wandosell, F., Camins, A., Carro, E., & Bartolome, F. (2022). Amyloid-β impairs mitochondrial dynamics and autophagy in Alzheimer's disease experimental models. Scientific Reports, 12(1), 10092. https://doi.org/10.1038/s41598-022-13683-3. De Duve, C., & Wattiaux, R. (1966). Functions of lysosomes. Annual Review of Physiology, 28(1), 435-492. Deng, M., Huang, L., Ning, B., Wang, N., Zhang, Q., Zhu, C., & Fang, Y. (2016). β-asarone improves learning and memory and reduces acetyl cholinesterase and beta-amyloid 42 levels in APP/PS1 transgenic mice by regulating Beclin-1-dependent autophagy. Brain Research, 1652, 188-194. Dineley, K. T., Hogan, D., Zhang, W.-R., & Taglialatela, G. (2007). Acute inhibition of calcineurin restores associative learning and memory in Tg2576 APP transgenic mice. Neurobiology of Learning and Memory, 88(2), 217-224. Do, K., Laing, B. T., Landry, T., Bunner, W., Mersaud, N., Matsubara, T., Li, P., Yuan, Y., Lu, Q., & Huang, H. (2018). The effects of exercise on hypothalamic neurodegeneration of Alzheimer's disease mouse model. PLoS One, 13(1), e0190205. https://doi.org/10.1371/journal.pone.0190205. Dong, Y., Li, X., Cheng, J., & Hou, L. (2019). Drug development for Alzheimer's disease: Microglia induced neuroinflammation as a target? International Journal of Molecular Sciences, 20(3), 558. https://doi.org/10.3390/ijms20030558. Gauthier, S., Rosa-Neto, P., Morais, J., & Webster, C. (2021). World Alzheimer report 2021: Journey through the diagnosis of dementia. Alzheimer's Disease International, 17-29. Gottlieb, R. A., & Carreira, R. S. (2010). Autophagy in health and disease. 5. Mitophagy as a way of life. American Journal of Physiology-Cell Physiology, 299(2), C203-C210. Grienberger, C., Rochefort, N. L., Adelsberger, H., Henning, H. A., Hill, D. N., Reichwald, J., Staufenbiel, M., & Konnerth, A. (2012). Staged decline of neuronal function in vivo in an animal model of Alzheimer's disease. Nature Communications, 3, 774. Guerchet, M., Prince, M., & Prina, M. (2020). Numbers of people with dementia worldwide: An update to the estimates in the World Alzheimer Report 2015. Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., & Iwatsubo, T. (2021). The amyloid-β pathway in Alzheimer's disease. Molecular Psychiatry, 26, 1-23. Hanson, C. D., & Clarke, C. (2013). Is expressed emotion related to estimates of ability made by older people with cognitive impairments and their partners? Aging & Mental Health, 17(5), 535-543. Hara, T., Nakamura, K., Matsui, M., Yamamoto, A., Nakahara, Y., Suzuki-Migishima, R., Yokoyama, M., Mishima, K., Saito, I., Okano, H., & Mizushima, N. (2006). Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice. Nature, 441(7095), 885-889. Hardy, J. A., & Higgins, G. A. (1992). Alzheimer's disease: The amyloid cascade hypothesis. Science, 256(5054), 184-185. He, C., & Klionsky, D. J. (2009). Regulation mechanisms and signaling pathways of autophagy. Annual Review of Genetics, 43, 67-93. He, C., Sumpter, R., Jr., & Levine, B. (2012). Exercise induces autophagy in peripheral tissues and in the brain. Autophagy, 8(10), 1548-1551. Hemming, M. L., & Selkoe, D. J. (2005). Amyloid β-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor. Journal of Biological Chemistry, 280(45), 37644-37650. Herrero-Mendez, A., Almeida, A., Fernández, E., Maestre, C., Moncada, S., & Bolaños, J. P. (2009). The bioenergetic and antioxidant status of neurons is controlled by continuous degradation of a key glycolytic enzyme by APC/C-Cdh1. Nature Cell Biology, 11(6), 747-752. Herring, A., Münster, Y., Metzdorf, J., Bolczek, B., Krüssel, S., Krieter, D., Yavuz, I., Karim, F., Roggendorf, C., Stang, A., Wang, Y., Hermann, D. M., Teuber-Hanselmann, S., & Keyvani, K. (2016). Late running is not too late against Alzheimer's pathology. Neurobiology of Disease, 94, 44-54. He, X.F., Liu, D., Zhang, Q., Liang, F., Dai, G., Zeng, J., Pei, Z., Xu, G., & Lan, Y. (2017). Voluntary exercise promotes glymphatic clearance of amyloid beta and reduces the activation of astrocytes and microglia in aged mice. Frontiers in Molecular Neuroscience, 10, 144. Huang, J., Wang, X., Zhu, Y., Li, Z., Zhu, Y. T., Wu, J. C., & Lin, F. (2019). Exercise activates lysosomal function in the brain through AMPK-SIRT1-TFEB pathway. CNS Neuroscience & Therapeutics, 25, 796-807. Huuha, A. M., Norevik, C. S., Moreira, J. B. N., Kobro-Flatmoen, A., Scrimgeour, N., Kivipelto, M., Van Praag, H., Ziaei, M., Sando, S. B., Wisløff, U., & Tari, A. R. (2022). Can exercise training teach us how to treat Alzheimer's disease? Ageing Research Reviews, 75, 101559. https://doi.org/10.1016/j.arr.2022.101559. Iliff, J. J., & Nedergaard, M. (2013). Is there a cerebral lymphatic system? Stroke, 44(6_Suppl. 1), S93-S95. Ittner, L. M., Ke, Y. D., Delerue, F., Bi, M., Gladbach, A., van Eersel, J., Wölfing, H., Chieng, B. C., Christie, M. J., Napier, I. A., Eckert, A., Staufenbiel, M., Hardeman, E., & Götz, J. (2010). Dendritic function of tau mediates amyloid-β toxicity in Alzheimer's disease mouse models. Cell, 142(3), 387-397. Iyaswamy, A., Wang, X., Krishnamoorthi, S., Kaliamoorthy, V., Sreenivasmurthy, S. G., Kumar Durairajan, S. S., Song, J. X., Tong, B. C., Zhu, Z., Su, C. F., Liu, J., Cheung, K. H., Lu, J. H., Tan, J. Q., Li, H. W., Wong, M. S., & Li, M. (2022). Theranostic F-SLOH mitigates Alzheimer's disease pathology involving TFEB and ameliorates cognitive functions in Alzheimer's disease models. Redox Biology, 51, 102280. Jansen, W. J., Ossenkoppele, R., Knol, D. L., Tijms, B. M., Scheltens, P., Verhey, F. R. J., Visser, P. J., Aalten, P., Aarsland, D., Alcolea, D., Alexander, M., Almdahl, I. S., Arnold, S. E., Baldeiras, I., Barthel, H., van Berckel, B. N. M., Bibeau, K., Blennow, K., Brooks, D. J., … Zetterberg, H. (2015). Prevalence of cerebral amyloid pathology in persons without dementia: A meta-analysis. Journal of the American Medical Association, 313(19), 1924-1938. Jian, Y., Yuan, S., Yang, J., Lei, Y., Li, X., & Liu, W. (2022). Aerobic exercise alleviates abnormal autophagy in brain cells of APP/PS1 mice by upregulating AdipoR1 levels. International Journal of Molecular Sciences, 23(17), 9921. https://doi.org/10.3390/ijms23179921. Jia, R., Liang, J., Xu, Y., & Wang, Y. (2019). Effects of physical activity and exercise on the cognitive function of patients with Alzheimer disease: A meta-analysis. BMC Geriatrics, 19(1), 181. Kanemitsu, H., Tomiyama, T., & Mori, H. (2003). Human neprilysin is capable of degrading amyloid β peptide not only in the monomeric form but also the pathological oligomeric form. Neuroscience Letters, 350(2), 113-116. Kayyali, U. S., Zhang, W., Yee, A. G., Seidman, J. G., & Potter, H. (1997). Cytoskeletal changes in the brains of mice lacking calcineurin Aα. Journal of Neurochemistry, 68(4), 1668-1678. Khorrami, A., Ghanbarzadeh, S., Mahmoudi, J., Nayebi, A., Maleki-Dizaji, N., & Garjani, A. (2015). Investigation of the memory impairment in rats fed with oxidized-cholesterol-rich diet employing passive avoidance test. Drug Research, 65(05), 231-237. Komatsu, M., Waguri, S., Chiba, T., Murata, S., Iwata, J., Tanida, I., Ueno, T., Koike, M., Uchiyama, Y., Kominami, E., & Tanaka, K. (2006). Loss of autophagy in the central nervous system causes neurodegeneration in mice. Nature, 441(7095), 880-884. LaFerla, F. M., Green, K. N., & Oddo, S. (2007). Intracellular amyloid-β in Alzheimer's disease. Nature Reviews Neuroscience, 8(7), 499-509. Lee, S., Sato, Y., & Nixon, R. A. (2011). Lysosomal proteolysis inhibition selectively disrupts axonal transport of degradative organelles and causes an Alzheimer's-like axonal dystrophy. The Journal of Neuroscience, 31(21), 7817-7830. Lin, M. T., & Beal, M. F. (2006). Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature, 443(7113), 787-795. Liu, F., Grundke-Iqbal, I., Iqbal, K., & Gong, C. X. (2005). Contributions of protein phosphatases PP1, PP2A, PP2B and PP5 to the regulation of tau phosphorylation. European Journal of Neuroscience, 22(8), 1942-1950. Liu, H.I., Zhao, G., Zhang, H., & Shi, L. (2013). Long-term treadmill exercise inhibits the progression of Alzheimer's disease-like neuropathology in the hippocampus of APP/PS1 transgenic mice. Behavioural Brain Research, 256, 261-272. Liu, Y., Fiskum, G., & Schubert, D. (2002). Generation of reactive oxygen species by the mitochondrial electron transport chain. Journal of Neurochemistry, 80(5), 780-787. López-Ortiz, S., Valenzuela, P. L., Seisdedos, M. M., Morales, J. S., Vega, T., Castillo-García, A., Nisticò, R., Mercuri, N. B., Lista, S., Lucia, A., & Santos-Lozano, A. (2021). Exercise interventions in Alzheimer's disease: A systematic review and meta-analysis of randomized controlled trials. Ageing Research Reviews, 72, 101479. https://doi.org/10.1016/j.arr.2021.101479. Luzio, J. P., Pryor, P. R., & Bright, N. A. (2007). Lysosomes: Fusion and function. Nature Reviews Molecular Cell Biology, 8(8), 622-632. Mansueto, G., Armani, A., Viscomi, C., D'Orsi, L., De Cegli, R., Polishchuk, E. V., Lamperti, C., Di Meo, I., Romanello, V., Marchet, S., Saha, P. K., Zong, H., Blaauw, B., Solagna, F., Tezze, C., Grumati, P., Bonaldo, P., Pessin, J. E., Zeviani, M., … Ballabio, A. (2017). Transcription factor EB controls metabolic flexibility during exercise. Cell Metabolism, 25(1), 182-196. Mansuy, I. M. (2003). Calcineurin in memory and bidirectional plasticity. Biochemical and Biophysical Research Communications, 311(4), 1195-1208. Marques-Aleixo, I., Santos-Alves, E., Balça, M. M., Rizo-Roca, D., Moreira, P. I., Oliveira, P. J., Magalhães, J., & Ascensão, A. (2015). Physical exercise improves brain cortex and cerebellum mitochondrial bioenergetics and alters apoptotic, dynamic and auto (mito) phagy markers. Neuroscience, 301, 480-495. Martini-Stoica, H., Xu, Y., Ballabio, A., & Zheng, H. (2016). The autophagy-lysosomal pathway in neurodegeneration: A TFEB perspective. Trends in Neurosciences, 39(4), 221-234. Mawuenyega, K. G., Sigurdson, W., Ovod, V., Munsell, L., Kasten, T., Morris, J. C., Yarasheski, K. E., & Bateman, R. J. (2010). Decreased clearance of CNS β-amyloid in Alzheimer's disease. Science, 330(6012), 1774. Medina, D. L., Di Paola, S., Peluso, I., Armani, A., De Stefani, D., Venditti, R., Montefusco, S., Scotto-Rosato, A., Prezioso, C., Forrester, A., Settembre, C., Wang, W., Gao, Q., Xu, H., Sandri, M., Rizzuto, R., De Matteis, M. A., & Ballabio, A. (2015). Lysosomal calcium signalling regulates autophagy through calcineurin and TFEB. Nature Cell Biology, 17(3), 288-299. Mehan, S., Arora, R., Sehgal, V., Sharma, D., & Sharma, G. (2012). Dementia-A complete literature review on various mechanisms involves in pathogenesis and an intracerebroventricular streptozotocin induced Alzheimer's disease, Inflammatory diseases-immunopathology, clinical and pharmacological bases. IntechOpen. Moreira, P. I., Carvalho, C., Zhu, X., Smith, M. A., & Perry, G. (2010). Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1802(1), 2-10. Moreira, P. I., Santos, M. S., & Oliveira, C. R. (2007). Alzheimer's disease: A lesson from mitochondrial dysfunction. Antioxidants & Redox Signaling, 9(10), 1621-1630. Moser, E. I., Krobert, K. A., Moser, M.-B., & Morris, R. G. M. (1998). Impaired spatial learning after saturation of long-term potentiation. Science, 281(5385), 2038-2042. Nilsson, P., & Saido, T. C. (2014). Dual roles for autophagy: degradation and secretion of Alzheimer's disease Aβ peptide. BioEssays, 36(6), 570-578. Nixon, R. A. (2013). The role of autophagy in neurodegenerative disease. Nature Medicine, 19(8), 983-997. Nixon, R. A. (2017). Amyloid precursor protein and endosomal-lysosomal dysfunction in Alzheimer's disease: Inseparable partners in a multifactorial disease. The FASEB Journal, 31(7), 2729-2743. Nixon, R. A., Wegiel, J., Kumar, A., Yu, W. H., Peterhoff, C., Cataldo, A., & Cuervo, A. M. (2005). Extensive involvement of autophagy in Alzheimer disease: An immuno-electron microscopy study. Journal of Neuropathology and Experimental Neurology, 64(2), 113-122. Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., Chiba, S., Atwood, C. S., Petersen, R. B., & Smith, M. A. (2001). Oxidative damage is the earliest event in Alzheimer disease. Journal of Neuropathology and Experimental Neurology, 60(8), 759-767. Nussbaum, J. M., Seward, M. E., & Bloom, G. S. (2013). Alzheimer disease: A tale of two prions. Prion, 7(1), 14-19. Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003). Triple-transgenic model of Alzheimer's disease with plaques and tangles. Neuron, 39(3), 409-421. Oddo, S., Caccamo, A., Smith, I. F., Green, K. N., & LaFerla, F. M. (2006). A dynamic relationship between intracellular and extracellular pools of Aβ. The American Journal of Pathology, 168(1), 184-194. Osellame, L. D., & Duchen, M. R. (2014). Quality control gone wrong: Mitochondria, lysosomal storage disorders and neurodegeneration. British Journal of Pharmacology, 171(8), 1958-1972. Palmieri, M., Impey, S., Kang, H., di Ronza, A., Pelz, C., Sardiello, M., & Ballabio, A. (2011). Characterization of the CLEAR network reveals an integrated control of cellular clearance pathways. Human Molecular Genetics, 20(19), 3852-3866. Palmieri, M., Pal, R., Nelvagal, H. R., Lotfi, P., Stinnett, G. R., Seymour, M. L., Chaudhury, A., Bajaj, L., Bondar, V. V., Bremner, L., Saleem, U., Tse, D. Y., Sanagasetti, D., Wu, S. M., Neilson, J. R., Pereira, F. A., Pautler, R. G., Rodney, G. G., Cooper, J. D., & Sardiello, M. (2017). mTORC1-independent TFEB activation via Akt inhibition promotes cellular clearance in neurodegenerative storage diseases. Nature Communications, 8, 14338. Polito, V. A., Li, H., Martini-Stoica, H., Wang, B., Yang, L., Xu, Y., Swartzlander, D. B., Palmieri, M., Ronza, A., Lee, V. M. Y., Sardiello, M., Ballabio, A., & Zheng, H. (2014). Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB. EMBO Molecular Medicine, 6(9), 1142-1160. Przedborski, S., Vila, M., & Jackson-Lewis, V. (2003). Series introduction: Neurodegeneration: What is it and where are we? Journal of Clinical Investigation, 111(1), 3-10. Rai, S. N., Tiwari, N., Singh, P., Mishra, D., Singh, A. K., Hooshmandi, E., Vamanu, E., & Singh, M. P. (2021). Therapeutic potential of vital transcription factors in Alzheimer's and Parkinson's disease with particular emphasis on transcription factor EB mediated autophagy. Frontiers in Neuroscience, 15, 777347. https://doi.org/10.3389/fnins.2021.777347. Reddy, K., Cusack, C. L., Nnah, I. C., Khayati, K., Saqcena, C., Huynh, T. B., Noggle, S. A., Ballabio, A., & Dobrowolski, R. (2016). Dysregulation of nutrient sensing and CLEARance in presenilin deficiency. Cell Reports, 14(9), 2166-2179. Rubinsztein, D. C., Codogno, P., & Levine, B. (2012). Autophagy modulation as a potential therapeutic target for diverse diseases. Nature Reviews Drug Discovery, 11(9), 709-730. Rusnak, F., & Mertz, P. (2000). Calcineurin: Form and function. Physiological Reviews, 80, 1483-1521. Sardiello, M. (2016). Transcription factor EB: From master coordinator of lysosomal pathways to candidate therapeutic target in degenerative storage diseases. Annals of the New York Academy of Sciences, 1371(1), 3-14. Sardiello, M., Palmieri, M., di Ronza, A., Medina, D. L., Valenza, M., Gennarino, V. A., Di Malta, C., Donaudy, F., Embrione, V., Polishchuk, R. S., Banfi, S., Parenti, G., Cattaneo, E., & Ballabio, A. (2009). A gene network regulating lysosomal biogenesis and function. Science, 325(5939), 473-477. Settembre, C., Di Malta, C., Polito, V. A., Arencibia, M. G., Vetrini, F., Erdin, S., Erdin, S. U., Huynh, T., Medina, D., Colella, P., Sardiello, M., Rubinsztein, D. C., & Ballabio, A. (2011). TFEB links autophagy to lysosomal biogenesis. Science, 332(6036), 1429-1433. Settembre, C., Fraldi, A., Medina, D. L., & Ballabio, A. (2013). Signals from the lysosome: A control centre for cellular clearance and energy metabolism. Nature Reviews Molecular Cell Biology, 14(5), 283-296. Settembre, C., Zoncu, R., Medina, D. L., Vetrini, F., Erdin, S., Erdin, S., Huynh, T., Ferron, M., Karsenty, G., Vellard, M. C., Facchinetti, V., Sabatini, D. M., & Ballabio, A. (2012). A lysosome-to-nucleus signalling mechanism senses and regulates the lysosome via mTOR and TFEB. The EMBO Journal, 31(5), 1095-1108. Shibata, M., Yamada, S., Kumar, S. R., Calero, M., Bading, J., Frangione, B., Holtzman, D. M., Miller, C. A., Strickland, D. K., Ghiso, J., & Zlokovic, B. V. (2000). Clearance of Alzheimer's amyloid-β 1-40 peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier. Journal of Clinical Investigation, 106(12), 1489-1499. Solé-Domènech, S., Cruz, D. L., Capetillo-Zarate, E., & Maxfield, F. R. (2016). The endocytic pathway in microglia during health, aging and Alzheimer's disease. Ageing Research Reviews, 32, 89-103. Song, J.-X., Liu, J., Jiang, Y., Wang, Z.-Y., & Li, M. (2021). Transcription factor EB: An emerging drug target for neurodegenerative disorders. Drug Discovery Today, 26(1), 164-172. Song, J. X., Malampati, S., Zeng, Y., Durairajan, S. S. K., Yang, C. B., Tong, B. C. K., Iyaswamy, A., Shang, W. B., Sreenivasmurthy, S. G., Zhu, Z., Cheung, K. H., Lu, J. H., Tang, C., Xu, N., & Li, M. (2020). A small molecule transcription factor EB activator ameliorates beta-amyloid precursor protein and Tau pathology in Alzheimer's disease models. Aging Cell, 19(2), e13069. https://doi.org/10.1111/acel.13069. Song, T. T., Cai, R. S., Hu, R., Xu, Y. S., Qi, B. N., & Xiong, Y. A. (2021). The important role of TFEB in autophagy-lysosomal pathway and autophagy-related diseases: A systematic review. European Review for Medical and Pharmacological Sciences, 25(3), 1641-1649. https://doi.org/10.26355/eurrev_202102_24875. De Sousa, R. A. L., Rodrigues, C. M., Mendes, B. F., Improta-Caria, A. C., Peixoto, M. F. D., & Cassilhas, R. C. (2021). Physical exercise protocols in animal models of Alzheimer's disease: A systematic review. Metabolic Brain Disease, 36(1), 85-95. https://doi.org/10.1007/s11011-020-00633-z. Sun, X., Chen, W.-D., & Wang, Y.-D. (2015). β-Amyloid: The key peptide in the pathogenesis of Alzheimer's disease. Frontiers in Pharmacology, 6, 221. Szegeczki, V., Horváth, G., Perényi, H., Tamás, A., Radák, Z., Ábrahám, D., Zákány, R., Reglodi, D., & Juhász, T. (2020). Alzheimer's disease mouse as a model of testis degeneration. International Journal of Molecular Sciences, 21(16), 5726. Szegeczki, V., Perényi, H., Horváth, G., Hinnah, B., Tamás, A., Radák, Z., Ábrahám, D., Zákány, R., Reglodi, D., & Juhász, T. (2021). Physical training inhibits the fibrosis formation in Alzheimer's disease kidney influencing the TGFβ signaling pathways. Journal of Alzheimer's Disease, 81(3), 1195-1209. Taglialatela, G., Hogan, D., Zhang, W.-R., & Dineley, K. T. (2009). Intermediate-and long-term recognition memory deficits in Tg2576 mice are reversed with acute calcineurin inhibition. Behavioural Brain Research, 200(1), 95-99. Tampellini, D., Rahman, N., Lin, M. T., Capetillo-Zarate, E., & Gouras, G. K. (2011). Impaired β-amyloid secretion in Alzheimer's disease pathogenesis. The Journal of Neuroscience, 31(43), 15384-15390. Tiribuzi, R., Crispoltoni, L., Porcellati, S., Di Lullo, M., Florenzano, F., Pirro, M., Bagaglia, F., Kawarai, T., Zampolini, M., Orlacchio, A., & Orlacchio, A. (2014). miR128 up-regulation correlates with impaired amyloid β (1-42) degradation in monocytes from patients with sporadic Alzheimer's disease. Neurobiology of Aging, 35(2), 345-356. Uddin, M. S., Stachowiak, A., Mamun, A. A., Tzvetkov, N. T., Takeda, S., Atanasov, A. G., Bergantin, L. B., Abdel-Daim, M. M., & Stankiewicz, A. M. (2018). Autophagy and Alzheimer's disease: From molecular mechanisms to therapeutic implications. Frontiers in Aging Neuroscience, 10, 04. Weller, R. O., Subash, M., Preston, S. D., Mazanti, I., & Carare, R. O. (2008). SYMPOSIUM: Clearance of Aβ from the brain in Alzheimer's disease: Perivascular drainage of amyloid-β peptides from the brain and its failure in cerebral amyloid angiopathy and Alzheimer's disease: Perivascular drainage of Aβ peptides and cerebral amyloid angiopathy. Brain Pathology, 18(2), 253-266. WHO. (2012). Alzheimer's disease international. Dementia: A public health priority. World Health Organization. Wirths, O., & Bayer, T. A. (2012). Intraneuronal Aβ accumulation and neurodegeneration: Lessons from transgenic models. Life Sciences, 91(23−24), 1148-1152. Xiao, Q., Yan, P., Ma, X., Liu, H., Perez, R., Zhu, A., Gonzales, E., Burchett, J. M., Schuler, D. R., Cirrito, J. R., Diwan, A., & Lee, J. M. (2014). Enhancing astrocytic lysosome biogenesis facilitates Aβ clearance and attenuates amyloid plaque pathogenesis. Journal of Neuroscience, 34(29), 9607-9620. Xiao, Q., Yan, P., Ma, X., Liu, H., Perez, R., Zhu, A., Gonzales, E., Tripoli, D. L., Czerniewski, L., Ballabio, A., Cirrito, J. R., Diwan, A., & Lee, J. M. (2015). Neuronal-targeted TFEB accelerates lysosomal degradation of APP, reducing Aβ generation and amyloid plaque pathogenesis. The Journal of Neuroscience, 35(35), 12137-12151. Yin, K.-J., Cirrito, J. R., Yan, P., Hu, X., Xiao, Q., Pan, X., Bateman, R., Song, H., Hsu, F. F., Turk, J., Xu, J., Hsu, C. Y., Mills, J. C., Holtzman, D. M., & Lee, J. M. (2006). Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-β peptide catabolism. The Journal of Neuroscience, 26(43), 10939-10948. Zeng, H., Chattarji, S., Barbarosie, M., Rondi-Reig, L., Philpot, B. D., Miyakawa, T., Bear, M. F., & Tonegawa, S. (2001). Forebrain-specific calcineurin knockout selectively impairs bidirectional synaptic plasticity and working/episodic-like memory. Cell, 107(5), 617-629. Zhang, Y., & Zhao, J. (2015). TFEB participates in the Aβ-induced pathogenesis of Alzheimer's disease by regulating the autophagy-lysosome pathway. DNA and Cell Biology, 34(11), 661-668. Zhao, N., Yan, Q.-W., Xia, J., Zhang, X.-L., Li, B.-X., Yin, L.-Y., & Xu, B. (2020). Treadmill exercise attenuates Aβ-induced mitochondrial dysfunction and enhances mitophagy activity in APP/PS1 transgenic mice. Neurochemical Research, 45(5), 1202-1214. Zhao, N., Zhang, X., Song, C., Yang, Y., He, B., & Xu, B. (2018). The effects of treadmill exercise on autophagy in hippocampus of APP/PS1 transgenic mice. Neuroreport, 29(10), 819-825. Zheng, L., Terman, A., Hallbeck, M., Dehvari, N., Cowburn, R. F., Benedikz, E., Kågedal, K., Cedazo-Minguez, A., & Marcusson, J. (2011). Macroautophagy-generated increase of lysosomal amyloid β-protein mediates oxidant-induced apoptosis of cultured neuroblastoma cells. Autophagy, 7(12), 1528-1545. Zhuo, M., Zhang, W., Son, H., Mansuy, I., Sobel, R. A., Seidman, J., & Kandel, E. R. (1999). A selective role of calcineurin Aα in synaptic depotentiation in hippocampus. Proceedings of the National Academy of Sciences, 96(8), 4650-4655. Zhu, S., Yao, R., Li, Y., Zhao, P., Ren, C., Du, X., & Yao, Y. (2021). The role and regulatory mechanism of transcription factor EB in health and diseases. Frontiers in Cell and Developmental Biology, 9, 667750. https://doi.org/10.3389/fcell.2021.667750. Zuroff, L., Daley, D., Black, K. L., & Koronyo-Hamaoui, M. (2017). Clearance of cerebral Aβ in Alzheimer's disease: Reassessing the role of microglia and monocytes. Cellular and Molecular Life Sciences, 74(12), 2167-2201.
فهرسة مساهمة:	Keywords: Alzheimer; TFEB; autophagy; brain; exercise
المشرفين على المادة:	0 (Amyloid beta-Peptides) 0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors) 0 (TFEB protein, human)
تواريخ الأحداث:	Date Created: 20230404 Date Completed: 20230530 Latest Revision: 20230530
رمز التحديث:	20231215
DOI:	10.1002/jcp.31005
PMID:	37013375
قاعدة البيانات:	MEDLINE

View record at Wiley

Full Text Finder

الوصف
تدمد:	1097-4652
DOI:	10.1002/jcp.31005