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Xiaolai Zhou
Xiaolai Zhou

Dr. Xiaolai Zhou is a Professor of Ophthalmology and a Principal Investigator of the Neuro-Ophthalmology Lab in the State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University (SYSU). Dr. Zhou received his M.D. from Hengyang Medical School, University of South China (2006) and Master's Degree in Ophthalmology from Zhongshan Ophthalmic Center, SYSU (2009). He obtained his Ph.D. in Neurobiology in Dr. Kerstin Krieglstein’s lab (2013) at the Department of Anatomy and Cell Biology in University of Freiburg, Germany, and conducted his postdoctoral training in Dr. Fenghua Hu’s lab at Weill Institute for Molecular & Cell Biology, Cornell University (2013-2017). Immediately after his postdoctoral training, Dr. Zhou joined Mayo Clinic (Jacksonville) as an Assistant Professor, where he worked closely with Dr. Rosa Rademakers, Dr. Dennis Dickson, and Dr. Guojun Bu. In December 2020, Dr. Zhou accepted the ‘Bairen’ professorship of Sun Yat-sen University, set up his research lab in the State Key Laboratory of Ophthalmology in Zhongshan Ophthalmic Center.

7 Jinsui Road, Tianhe District, Guangzhou PRC

Clinical and Basical Research:
Dr. Zhou worked on the molecular and genetic mechanisms of lysosomal dysfunction related-brain and -retinal degeneration. Specifically, his research focused on frontotemporal lobar degeneration and retinal degeneration caused by Progranulin (PGRN) gene mutation. Dr. Zhou’s research has been published in peer-review journals, such as Lancet Neurol., Nat Commun., Brain, Acta Neuropathol., J Cell Biology, EMBO Rep.

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Research Projects

Dr. Zhou’s lab is currently focusing on the following three topics:
1.      Disease mechanism and clinical diagnosis and treatment of neuromyelitis optica spectrum disorder (NMOSD).
2.      Molecular mechanism of lysosomal dysfunction related-neurodegenerative diseases such as frontotemporal lobar degeneration (FTLD) and retinal degeneration caused by progranulin (PGRN) mutation.
3.      Gene therapy for retinal degeneration and optic nerve atrophy.

Selected recent publications


1.      Zhou X, Kukar T, Rademakers R. Lysosomal Dysfunction and Other Pathomechanisms in FTLD: Evidence from Progranulin Genetics and Biology. Adv Exp Med Biol. 2021;1281:219-242. doi: 10.1007/978-3-030-51140-1_14.

2.      Zhou X#, Brooks M, Jiang P, Koga S, Zuberi A, Baker M, Parsons T, Castanedes-Casey M, Phillips V, Librero A, Kurti A, Fryer J, Bu G, Lutz C, Dickson D#, and Rademakers R#. Loss of Tmem106b exacerbates FTD pathologies and causes motor deficits in progranulin deficient mice. EMBO Reports. 2020 Aug 5;21(10): e50197. # Corresponding author. Commented by EMBO Reports and ALZFORUM

3.      Zhou X#, Nicholson A, Ren Y, Brooks M, Jiang P, Zuberi A, Phuoc H, Perkerson R, Matchett B, Parsons T, Finch N, Lin W, Qiao W, Castanedes-Casey M, Phillips V, Librero A, Asmann Y, Bu G, Murray M, Lutz C, Dickson D, and Rademakers R#. Loss of Tmem106b leads to myelination deficits: implications for FTD treatment strategies. Brain. 2020. Jun 1;143(6):1905-1919. # Corresponding author. Commented by Brain

4.      Nicholson A*, Zhou X *, Perkerson R., Parsons T, Chew J, Brooks M, DeJesus-Hernandez M, Matchett B, Kurti A, Zhou W, Tian S, Castanedes-Casey M, Rousseau L, Phillips V, Murray M, Dickson DW, Fryer JD, Petrucelli L, Rademakers R. Loss of Tmem106b is unable to ameliorate frontotemporal dementia-like phenotypes in an AAV mouse model of C9ORF72-repeat induced toxicity. Acta Neuropathol Commun. 2018 May 31;6(1):42. * Equal contribution.

5.      Pottier C*, Zhou X*, Perkerson RB 3rd, Baker M, ….Rademakers R. Potential genetic modifiers of disease risk and age at onset in patients with frontotemporal lobar degeneration and GRN mutations: a genome-wide association study. Lancet Neurol. 2018 Jun;17(6):548-558. Commented by The Lancet Neurology. * Equal contribution.

6.      Zhou X, Rademakers R. TMEM106B and myelination: rare leukodystrophy families reveal unexpected connections. Brain. 2017 Dec 1;140(12):3069-3080.

7.      Zhou X*, Paushter DH*, Feng T, Sun L, Reinheckel T, Hu F. Lysosomal processing of progranulin. Mol Neurodegener. 2017 Aug 23;12(1):62. *Equal contribution. Commented by ALZFORUM. progranulin-and-lysosome-function.

8.      Zhou X*, Sullivan PM*, Sun L, Hu F. The interaction between progranulin and prosaposin is mediated by granulins and the linker region between saposin B and C. J Neurochem. 2017 Jun 22. *Equal contribution. Editorial comment in the issue.

9.      Zhou X, Sun L, Bracko O, Choi JW, Jia Y, Nana AL, Brady OA, Hernandez JCC, Nishimura N, Seeley WW, Hu F. Impaired prosaposin lysosomal trafficking in frontotemporal lobar degeneration due to progranulin mutations. Nat Commun. 2017 May 25;8:15277

10.  Zhou X, Paushter DH, Feng T, Pardon CM, Mendoza CS, Hu F. Regulation of cathepsin D activity by the FTLD protein progranulin. Acta Neuropathol. 2017 Jul;134(1):151-153.

11.  Zhou X*, Sun L*, Brady OA, Murphy KA, Hu F. Elevated TMEM106B levels exaggerate lipofuscin accumulation and lysosomal dysfunction in aged mice with progranulin deficiency. Acta Neuropathol Commun. 2017 Jan 26;5(1):9. * Equal contribution.

12.  Zhou X, Sun L, Qi X, Oliveira F, Brown WJ, Smolka M, Sun Y, Hu F. Prosaposin facilitates sortilin independent lysosomal targeting of progranulin. J Cell Biology. 2015 Sep 14; 210 (6). Highlighted in the issue.

13.  Zhou X, Z?ller T, Krieglstein K, Spittau B. TGFβ1 inhibits IFNγ-mediated microglia activation and protects mDA neurons from IFNγ-driven neurotoxicity. J Neurochem. 2015 Mar 31; 134 (1), 125-134.

14.  Zhou X, Spittau B, Krieglstein K. TGF-beta signaling plays an important role in IL4-induced alternative activation of microglia. J Neuroinflammation. 2012 Sep 4; 9(1):210.