Waldo Herrera
University of Pennsylvania
6 Papers
83 Citations
Waldo Herrera is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Retina & Retinal. The author has an hindex of 6, co-authored 6 publications.
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Papers
CERKL mutations cause an autosomal recessive cone-rod dystrophy with inner retinopathy.
Tomas S. Aleman,Nagasamy Soumittra,Artur V. Cideciyan,Alexander Sumaroka,Vedam L. Ramprasad,Waldo Herrera,Elizabeth A. M. Windsor,Sharon B. Schwartz,Robert C. Russell,Alejandro J. Roman,Chris F. Inglehearn,Govindasamy Kumaramanickavel,Edwin M. Stone,Gerald A. Fishman,Samuel G. Jacobson +14 more
TL;DR: CERKL mutations are associated with widespread retinal degeneration with prominent maculopathy and the clinical presentation is that of an autosomal recessive cone-rod dystrophy.
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Retinal disease in Usher syndrome III caused by mutations in the clarin-1 gene.
Waldo Herrera,Tomas S. Aleman,Artur V. Cideciyan,Alejandro J. Roman,Eyal Banin,Tamar Ben-Yosef,Leigh M. Gardner,Alexander Sumaroka,Elizabeth A. M. Windsor,Sharon B. Schwartz,Edwin M. Stone,Xue Zhong Liu,William J. Kimberling,Samuel G. Jacobson +13 more
TL;DR: Comparisons between USH3A and USH2A suggested a common rod and cone phenotype but a more accelerated time course of rod loss in USH 3A, and peripheral function measurements showed USh3A to be more rapidly progressive than USh2A.
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•Journal Article
Leber congenital amaurosis caused by Lebercilin (LCA5) mutation: retained photoreceptors adjacent to retinal disorganization.
Samuel G. Jacobson,Tomas S. Aleman,Artur V. Cideciyan,Alexander Sumaroka,Sharon B. Schwartz,Elizabeth A. M. Windsor,Malgorzata Swider,Waldo Herrera,Edwin M. Stone +8 more
TL;DR: The NIR reflectance and NIR-AF imaging in the younger patient suggested preserved RPE in retinal regions with retained photoreceptors mainly in the central retina, and detailed phenotype studies in other LCA5 patients with longitudinal follow-up will help determine the feasibility of future intervention in this rare disease.
Normal central retinal function and structure preserved in retinitis pigmentosa.
Samuel G. Jacobson,Alejandro J. Roman,Tomas S. Aleman,Alexander Sumaroka,Waldo Herrera,Elizabeth A. M. Windsor,Lori A. Atkinson,Sharon B. Schwartz,Janet D. Steinberg,Artur V. Cideciyan +9 more
TL;DR: Unexpected was the observation that patients with presumed recessive RP can have regions with functionally and structurally normal retina, and will require special consideration in future clinical trials of either focal or systemic treatment.
Usher syndromes due to MYO7A, PCDH15, USH2A or GPR98 mutations share retinal disease mechanism
Samuel G. Jacobson,Samuel G. Jacobson,Artur V. Cideciyan,Tomas S. Aleman,Alexander Sumaroka,Alejandro J. Roman,Leigh M. Gardner,Haydn M. Prosser,Monalisa Mishra,N. Torben Bech-Hansen,Waldo Herrera,Sharon B. Schwartz,Xue Zhong Liu,William J. Kimberling,Karen P. Steel,David S. Williams +15 more
TL;DR: The results point to the photoreceptor cell as the therapeutic target for USH treatment trials, such as MYO7A somatic gene replacement therapy.