Publications

Glaucomatous optic neuropathy, or glaucoma, is the world's primary cause of irreversible blindness. Glaucoma is comorbid with other neurodegenerative diseases, but how it might impact the environment of the full central nervous system to increase neurodegenerative vulnerability is unknown. Two neurodegenerative events occur early in the optic nerve, the structural link between the retina and brain: loss of anterograde transport in retinal ganglion cell (RGC) axons and early alterations in astrocyte structure and function. Here, we used whole-mount tissue clearing of full mouse brains to image RGC anterograde transport function and astrocyte responses across retinorecipient regions early in a unilateral microbead occlusion model of glaucoma. Using light sheet imaging, we found that RGC projections terminating specifically in the accessory optic tract are the first to lose transport function. Although degeneration was induced in one retina, astrocytes in both brain hemispheres responded to transport loss in a retinotopic pattern that mirrored the degenerating RGCs. A subpopulation of these astrocytes in contact with large descending blood vessels were immunopositive for LCN2, a marker associated with astrocyte reactivity. Together, these data suggest that even early stages of unilateral glaucoma have broad impacts on the health of astrocytes across both hemispheres of the brain, implying a glial mechanism behind neurodegenerative comorbidity in glaucoma.

[This corrects the article 24 in vol. 14, PMID: 39234588.].

[This corrects the article on p. 4128 in vol. 13, PMID: 39629448.].

[Erratum to: BMB Reports 2024; 57(11): 497-502, PMID: 39384175, PMCID: PMC11608851] The BMB Reports would like to issue a correction to an article published in BMB Rep. 57(11): 497-502, titled "Differential roles of N- and C-terminal LIR motifs in the catalytic activity and membrane targeting of RavZ and ATG4B proteins". The original acknowledgment contained incorrect grant information. This has now been corrected at the authors' request as follows: The work was supported by the Science Research Center Program of the National Research Foundation NRF (2020R1A5A1019023); Neurological Disorder Research Program of the NRF (2020M3E5D9079911); Basic research program of the NRF (2023R1A2C2007082) to JAL. D.-J.J. was supported by the Basic Research Program of NRF (2022R1F1A1066552), and the NRF grant funded by the Korea government (MSIT) (RS-2023-00218515). Specifically, the grant number has been updated from [2023R1A2C2008092] to [2023R1A2C2007082]. The authors apologize for any inconvenience or confusion this error may have caused. The ACKNOWLEDGEMENTS section in the original PDF version has been updated accordingly.

[This retracts the article on p. 1354 in vol. 14, PMID: 39319232.].

The authors of the article titled "Advances in Genetic Reprogramming: Prospects from Developmental Biology to Regenerative Medicine" (Dhanjal DS, Singh R, Sharma V, Nepovimova E, Adam V, Kuca K, Chopra C. Curr Med Chem. 2024; 31(13): 1646-1690. DOI: 10.2174/0929867330666230503144619. PMID: 37138422) [1] have made revisions to the references in the text and the reference section. These updates have been made to ensure the integrity of the article. The updated reference list can be found in the latest version of the article. The authors apologize for any confusion or inconvenience caused. The original article can be found online at: https://www.eurekaselect.com/article/131443.

[This corrects the article on p. 2006 in vol. 16, PMID: 38764815.].

[This retracts the article on p. 509 in vol. 18, PMID: 39600461.].