University of Missouri School of Medicine MU Health School of Medicine
katz-ma

Martin L. Katz, PhD

Professor of Ophthalmology, Director Campus Electron Microscopy Core Facility

Background

  • B.S.: Marquette University (1974)
  • PhD: Biology (Biochemistry), University of California, Santa Cruz (1981)
  • Postdoctoral: National Eye Institute, Nation Institutes of Health

Click here to visit the Neurodegenerative Diseases Research Lab website

Honors and Other Special Recognition

  • Phi Beta Kappa
  • Graduated Summa Cum Laude, Marquette University
  • Marquette University Scholarships
  • University of California Graduate Fellowship
  • University of California Patent Fund Awards 1977, 1978
  • Fight for Sight Fellowships 1979, 1980
  • National Research Service Award 1981
  • Elected to Board of Directors, American Aging Association, 1985-1988; 1992-1998
  • Program Committee, American Aging Association, 1989-1995
  • University of Missouri Faculty Foreign Travel Award, 1990
  • Appointed to the doctoral faculty in Biological Sciences, University of Missouri 1992
  • Ad hoc member, Visual Sciences Study Section, National Institutes of Health, 1992-1993
  • Member of Scientific Review Board, Fight for Sight, Inc., 1993-1995
  • Temporary member, Medical Biochemistry Study Section, National Institutes of Health, 1997
  • International Advisory Committee, Sixth Symposium on Lipofuscin, 2001

Research Topics

Neurophysiology in Retinal Degenerative Diseases
Katz M Media 2-fluoresenceRPE
Figure 1: Fluorescence micrograph of the RPE from an old albino rat showing the substantial accumu-lation of lipofuscin, which emits a golden-yellow light when stimulated with blue light excitation. All of the yellow color is due to lipofuscin fluorescence.

The goals of research conducted in the laboratory of Professor Katz are to develop a better understanding of the mechanisms that underlie neurodegenerative disorders and to develop therapiesfor treating these disorders. The particular focus of the research is on age-related macular degeneration (ARMD) and hereditary ceroid-lipofuscinosis (CLN), also known as Batten disease. ARMD may result, at least in part, from a progressive age-related accumulation of lysosomal storage bodies, called lipofuscin, in the retinal pigment epithelium (RPE) (see Figure 1 below). The focus of Dr. Katz' ARMD research is to elucidate the cellular and molecular mechanisms of RPE lipofuscin formation. In particular, he is conducting studies to test the hypothesis that lipofuscin forms primarily by reactions between vitamin A aldehyde and the molecular constituents of the photoreceptor outer segments. CLN is a group of autosomal-recessive hereditary diseases that lead to blindness, neurological deterioration, and premature death. A major goal of his CLN research is to develop therapies to treat these disorders. Toward this end, Dr. Katz and his associates are currently using animal models to develop stem cell implantation (see Figure 2) and gene therapies for the CLNs.

Ceroid-Lipofuscinosis in Tibetan Terriers
Katz M Media 1-fluoresenceEGFP
Figure 2: Fluorescence micrographs showing EGFP expressing stem cells (green) after transplantation into the eyes of mice with inherited retinal degeneration. (A) Surface view of retina 4 days after transplant. (B) Cross-section of retina 4 days fter transplant. (C) Surface view of retina 6 weeks after transplant. (D) Cross-section of retina 6 weeks after transplant.

Ceroid-lipofuscinosis (CLN) occurs in a number of animal species in addition to humans. Animals in which CLN has been reported include a number of dog breeds, including Tibetan Terriers, English Setters, Polish Lowland Sheepdogs, and American Bulldogs. Dr. Katz and his colleagues have been conducting research to identify the genetic defects responsible for the CLN diseases in these and other dog breeds. They have recently identified the mutation responsible for the English Setter disorder. This finding will be published in early 2005 in the journal Biomchemical and Biophysical Research Communications. Individuals who have dogs that exhibit behavioral changes should consult the Canine Neuronal Ceroid Lipofuscinosis website for more information. As the canine disease genes are identified, Dr. Katz and colleagues will offer genetic testing for dog breeders and pet owners.

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Bone Marrow Derived Stem Cells for Treating Neurodegenerative Disorders
Katz M Media 3-mesenchymal-stem-cell
A murine mesenchymal stem cell cultured in media containing known neural growth factors. It displays a flattened cell body, extended morphology and upregulated expression of betaIII tubulin, a cytoskeletal protein expressed in neurons and visualized with immunolabeling for Texas Red.

Our laboratory, in collaboration with Mark Kirk and Gregory Tullis, is currently exploring the use of mesenchymal stem cells (MSCs), a subpopulation of cells derived from the bone marrow, as a method of enzyme delivery to mouse models of the neurodegenerative disease neuronal ceroid lipofuscinosis (NCL). MSCs have several advantages as cells for neurotransplantation. In particular, they can be readily obtained from bone marrow and expanded in culture, unlike the inaccessible neural stem cell sources deep in the brain. Also a patient’s own MSCs can be used, thus circumventing the problem of host immunity and graft versus host disease. If an accessible pluripotent stem cell source can be identified, autologous stem cell therapies offer a great advantage. We have preliminarily shown that in vitro culture of both murine derived MSCs and human bone marrow derived stem cells (Neuronyx) in media containing neural growth factors induces upregulation of cell surface markers commonly expressed on neurons. In addition, MSCs exposed to neural growth factors display a more neural morphology by flattening out and extending longer processes from the cell body. This leads us to believe that it may be possible to induce MSCs to differentiate into more neural-like cells prior to transplantation in vivo to promote long term engraftment of transplanted cells.

Recently, we have isolated MSCs from mice (Jackson Laboratory) that endogenously express green fluorescent protein (GFP). These cells are ideal for transplant studies, as donor MSCs can be tracked within the host after transplant and, through colabeling with known markers, provide information about their differentiation pathway in vivo. We have already transplanted GFP-expressing MSCs into the vitreous of the eye of the mnd mouse, a popular model for NCL. These studies indicate that the ocular environment may promote upregulation of mature neural markers, but long term engraftment is not seen. We continue to experiment with in vitro induction protocols to support in vivo engraftment of donor murine MSCs into the central nervous system of mouse models of NCL.

Research on ALS

Current and Previous Research Funding Sources

Research Training Opportunities

Dr. Katz is a member of the University doctoral faculty in Biological Sciences and of the graduate faculty in Genetics, Neuroscience and Pathobiology. There are currently openings in his laboratory in any of these areas for doctoral students who wish to focus on either the molecular genetics of inherited eye diseases or the biochemistry of age-related macular degeneration. For more information, please contact Dr. Katz by letter, fax or e-mail.

There are also openings in his lab for postdoctoral fellows in molecular biology with experience in PCR, RFLP, and protein analysis using gel electrophoresis and Western blotting. If interested, please send Dr. Katz a CV, a letter describing your research experience, and the names of three references.

Media

Feb. 11, 2013:

Effective Treatment for Late Infantile Batten Disease Developed by MU, BioMarin Researchers

Read more...

 

NPR:

Batten Disease Unites Parents, Dog Owners

Read more...

 

Publications

  1. Awano T, Johnson GS, Wade CM, Katz M L, Johnson GC, Taylor JF, Perloski M, Biagi T, Long S, March PA, Olby NJ, Khan S, O’Brien DP, Lindblad-Toh K and Coates JR. Genome-wide association analysis reveals a SOD1 mutation in Canine Degenerative Myelopathy: That Resembles Amyotrophic Lateral Sclerosis. Proc. Nat. Acad. Sci. USA. (http://dx.doi.org/10.1073/pnas.0812297106)
  2. Hainsworth DP, Liu G, Hamm CW and Katz M L: Funduscopic and Angiographic Appearance of Neuronal Ceroid Lipofuscinosis (Batten Disease). Retina, in press, 2008.
  3. Katz M L, Coates JR, Cooper JJ, O’Brien DP, Jeong M, and Narfström K: Retinal Pathology in a Canine Model of Late Infantile Neuronal Ceroid Lipofuscinosis. Invest. Ophthalmol. Vis. Sci. 49:2686-2695, 2008. (http://dx.doi.org/10.1167/iovs.08-1712)
  4. O’Brien DP and Katz M L: Neuronal ceroid lipofuscinosis in three Australian shepherd littermates. J. Vet. Internal Med. 22:472-475, 2008. (http://dx.doi.org/10.1111/j.1939-1676.2008.0079.x)
  5. Narfström K, Seeliger M, Lai CM, Vaegan, Katz M L, Rakoczy EP, Remé C. Morphological aspects related to long-term functional improvement of the retina in 4 years following rAAV-mediated gene transfer in the RPE65 null mutation dog. Adv. Exp. Med. Biol. 613:139-146, 2008.
  6. Chen X, Johnson GS, Schnabel RD, Taylor JF, Johnson GC, Parker HG, Patterson EE, Katz M L, Awano T, Khan S, O’Brien DP: A neonatal encephalopathy with seizures in standard poodle dogs with a missense mutation in the canine ortholog of ATF2. Neurogenetics 9:41-49, 2008. (http://dx.doi.org/10.1007/s10048-007-0112-2)
  7. Katz M L, Johnson GS, Tullis GE and Lei B: Phenotypic characterization of a mouse model of juvenile neuronal ceroid lipofuscinosis. Neurobiol. Dis. 29:242-253, 2008.
  8. Katz M L, Sanders DN, Mooney BP and Johnson GS: Accumulation of Glial fibrillary acidic protein and histone H4 in brain storage bodies of Tibetan Terriers with hereditary neuronal ceroid lipofuscinosis. J. Inherit. Metabol. Dis. 30:952-963, 2007.
  9. Pierret C, Spears, KM, Morrison J, Maruniak JA, Katz M L and Kirk MD: An in vitro neural stem cell niche derived from murine embryonic stem cells. Stem Cells Dev. 16:1-10, 2007.
  10. Awano T, Katz M L, Sohar I, Lobel P, Sanders DN, Khan S, Johnson GC, Giger U and Johnson GS: A frame shift mutation in the canine ortholog of human CLN2 in a juvenile dachshund with neuronal ceroid lipofuscinosis. Molec. Genet. Metab. 89:254-260, 2006.
  11. Lei B, Tullis GE, Kirk MD, Zhang K and Katz M L. Ocular Phenotype in a Mouse Gene Knockout Model for Infantile Neuronal Ceroid-Lipofuscinosis (CLN1). J Neurosci Res. 84:1139-1149, 2006.
  12. Awano T, Katz M L, O’Brien DP, Taylor JF, Evans J, Khan S, Lobel P, Sohar I, and Johnson GS. A mutation in the cathepsin D gene (CTSD) in American Bulldogs with neuronal ceroid-lipofuscinosis. Molec Genet Metab. 87:341-348, 2006.
  13. Meyer JS, Katz M L, Maruniak JA and Kirk MD. Embryonic stem cell derived neural precursors incorporate into the degenerating retina and enhance survival of host photoreceptors. Stem Cells. 24:274-283, 2006.
  14. Narfström K, Katz M L, Bragadottir R, Ford MM, Redmond TM, Lai MJT, Brankov M, Barnett NL, Moore SR, Stoddart CW, Martin-Iverson MT and Rakoczy PE. Partial recovery of retinal function in RPE65-/- mice and dogs following rAAV-mediated genetherapy. In: Redberry GW (ed.) Trends in Gene Therapy Research. Hauppauge, NY. Nova Science Publishers, pp. 129-145, 2005.
  15. Narfström K, Vaegan, Katz M L, Bragadottir R, Rakoczy EP and Seeliger M. Assessment of Structure and Function over a 3-Year Period after Gene Transfer in RPE65-/- Dogs. Doc Ophthalmol. 111:39-48, 2005.
  16. Meyer JS, Katz M L and Kirk MD. Stem cells and retinal degenerative disorders. Ann NY Acad Sci. 1049:135-145, 2005.
  17. Wendt, KD, Lei B, Schachtman TR, Tullis GE, Ibe ME, and Katz M L. Behavioral assessment of mouse models of ceroid-lipofuscinosis using a light-cued T-maze. Behav Brain Res. 161: 175-182, 2005.
  18. Katz M L, Wendt KD and Sanders DN. RPE65 gene mutation prevents development of autofluorescence in retinal pigment epithelial phagosomes. Mech Age Dev. 126:513-521, 2005.
  19. Evans J, Katz M L, Levesque D, Shelton D, deLahunta A and O’Brien DP. A Variant Form of Neuronal Ceroid Lipofuscinosis in American Bulldogs. J Vet Internal Med. 19: 44-51, 2005.
  20. Katz M L, Khan S, Awano T, Shahid A, Siakotos AN, Johnson GS. A mutation in the CLN8 gene in English Setter dogs with neuronal ceroid-lipofuscinosis. Biochem Biophys Res Commun. 327:541-547, 2005.
  21. Katz M L, Narfström K, Johnson GS, O’Brien DP. Assessment of retinal function and characterization of lysosomal storage body accumulation in the retinas and brains of Tibetan Terriers with ceroid-lipofuscinosis. Am J Vet Res. 66:67-76, 2005.
  22. Meyer JS, Katz M L, Maruniak JA, Kirk MD. Neural differentiation of mouse embryonic stem cells in vitro and after transplantation into the eyes of mice with rapid retinal degeneration. Brain Res. 1014:131-144, 2004.
  23. Wendt KD , Jensen CA, Tindall R, Katz M L. Comparison of conventional and microwave-assisted processing of mouse retinas for transmission electron microscopy. J Microscopy. Apr;214(Pt 1):80-8, 2004.
  24. Narfström K, Katz M L, Ford M, Redmond TM, Rakoczy E, Bragadóttir R. In vivo gene therapy in young and adult RPE65 dogs produces long-term visual improvement. J Heredity. 94:31-37, 2003.
  25. Narfström K, Katz M L, Bragadottir R, Seeliger M, Boulanger A, Redmond TM, Caro L, Lai C-M, Rakozcy E. Functional and structural recovery of the retina after gene therapy in the RPE65 null mutation dog. Invest Ophthalmol Vis Sci. 44:1663-1672, 2003.
  26. Hainsworth DP, Katz M L, Wright EJ, Sanders DA, Sanders DN, Sturek M. Retinal Capillary Basement Membrane Thickening in a Porcine Model of Diabetes. Comp Med. 52:523-529, 2002.
  27. Katz M L, Sanders DA, Sanders DN, Hansen E, Johnson GS. Assessment of Plasma Carnitine Concentration in Relation to Ceroid-Lipofuscinosis in Tibetan Terriers. Am J Veterinary Res. 63:890-895, 2002.
  28. Katz M L. Bernard Strehler: Inspiration for Basic Research into the Mechanisms of Aging. Mech Age Dev. 123:831-840, 2002.
  29. Katz M L. Potential reversibility of lipofuscin accumulation. Arch Gerontol. Geriatrics. 34:311-317, 2002.
  30. Katz M L, Robison WG. What is lipofuscin? Defining characteristics and differentiation from other autofluorescent lyososomal storage bodies. Arch Gerontol Geriatrics. 34:169-184, 2002.
  31. Katz M L. Potential role of retinal pigment epithelial lipofuscin accumulation in age-related macular degeneration. Arch Gerontol Geriatrics. 34:359-370, 2002.
  32. Katz M L, Redmond TM. Effect of Rpe65 knockout accumulation of lipofuscin fluorophores in the retinal pigment epithelium. Invest. Ophthalmol. Vis Sci. 42:3023-3030, 2001.
  33. Siakotos AN, Hutchins GD, Farlow MR, Katz M L. Assessment of dietary therapies in a canine model of Batten disease. Eur J Paediatr Neurol. 5A:151-156, 2001.
  34. Katz M L, Johnson GS. Mouse gene knockout models for the CLN2 and CLN3 forms of ceroid-lipofuscinosis. Eur J Paediatr Neurol. 5A:109-114, 2001.
  35. Katz M L, Shibuya H, Johnson GS. Animal models for the ceroid-lipofuscinoses. Adv Genetics. 45:183-203, 2001.
  36. Bensaoula T, Shibuya H, Katz M L, Smith JE, Johnson GS, John SK, Milam AH. Histopathologic and immunocytochemical analysis of the retina and ocular tissues in Batten disease. Ophthalmol. 107:1746-1753, 2000.
  37. Robison WG, Jacot JL, Katz M L, Glover JP. Retinal vascular changes induced by the oxidative stress of alpha-tocopherol deficiency contrasted with diabetic microangiopathy. J Ocular Pharmacol Therapeutics. 16:109-120, 2000.
  38. Hjelmeland LM, Cristofolo VJ, Funk W, Rakoczy E, Katz M L. Senescence of the RPE. Molecular Vision. 5:33, 1999.
  39. Katz M L, Liu P, Grob-Nunn S, Shibuya H, Johnson GS. Chracterization and chromosomal mapping of a mouse ortholog of the late-infantile ceroid-lipofuscinosis gene CLN2 . Mamm Genome. 10:1050-1053, 1999.
  40. Katz M L, Shibuya H, Liu P, Kaur S, Gao C, Johnson GS. A mouse gene knockout model for juvenile ceroid-lipofuscinosis. J Neurosci Res. 57:551-556, 1999.
  41. Katz M L, Gao C, Rice LM. Long-term variations in cyclic light intensity and dietary vitamin A intake modulate lipofuscin content of the retinal pigment epithelium. J Neurosci Res. 57:106-116, 1999.
  42. Riis R, Jackson C, Rebhun W, Katz M L, Loew E, Summers B, Cummings J, de LaHunta A, Divers T, Mohammed H. Ocular manifestations of equine motor neuron disease. Equine Veterinary J. 31:99-110, 1999.
  43. Katz M L, Rice LM, Gao C. Reversible Accumulation of lipofuscin-like inclusions in the retinal pigment epithelium. Invest Ophthalmol Vis Sci. 40:175-181, 1999.
  44. Ganjam KK, Shibuya H, Stoy SJ, Liu P, Ganjam VK, Katz M L, Johnson GJ. A BstU I marker in an intron of the canine fibrillin 1 gene. Animal Genet. 29:240-241, 1998.
  45. Liu P, Chen Y, Shibuya H, Katz M L, Lubahn DB, Johnson GS. A polymorphic (GA) n microsatellite in an intron of the canine endothelin-B receptor gene. Animal Genet. 29:236, 1998.
  46. Liu P, Shibuya H, Katz M L, Johnson GS. A Bsm FI PCR/RFLP in the canine CD19 gene. Animal Genet. 29:64-65, 1998.
  47. Shibuya H, Liu P, Katz M L, Siakotos AN, Nonneman DJ, Johnson GJ. Coding sequence and exon/intron organization of the canine CLN3 (Batten disease) gene and its exclusion as the locus for ceroid lipofuscinosis in English setter dogs. J Neurosci Res. 52:268-275, 1998.
  48. Liou GI, Matragoon S, Chen D, Gao C, Fei Y, Katz M L, Stark WS. Visual Sensitivity and Interphotoreceptor retinoid-binding protein in the mouse. FASEB J. 12:129-138, 1998.
  49. Siakotos AN, Blair PS, Savill JD, Katz M L. Altered mitochondrial function in canine ceroid-lipofuscinosis. Neurochem Res. 23:983-989, 1998.
  50. Katz M L, Gao C, Prabhakaram M, Liu P, Shibuya H, Johnson GS. Immunochemical localization of the Batten disease (CLN3) protein in retina. Invest Ophthalmol Vis Sci. 38:2373-2384, 1997.
  51. Katz M L, Rice LM, Gao C. Dietary carnitine supplements slow disease progression in a putative mouse model for hereditary ceroid-lipofuscinosis. J Neurosci Res. 50:123-132, 1997.
  52. Katz M L, Siakotos AN, Gao Q, Freiha B, Chin DT. Late-infantile ceroid-lipofuscinosis: lysine methylation of mitochondrial ATP synthase subunit c from lysosomal storage bodies. Biochim Biophys Acta. 1361:66-74, 1997.
  53. Katz M L, Gao C, Rice L M, Formation of Lipofuscin-like Fluorophores by Reaction of Retinal with Photoreceptor Outer Segments. Mech Age Dev. 92:159-174, 1996.
  54. Katz M L, Decreased Plasma Carnitine and Trimethyl-L-Lysine Levels Associated with Lysosomal Accumulation of a Trimethyl-L-Lysine Containing Protein in Batten Disease. Biochim Biophys Acta. 1317:192-198, 1996.
  55. Prabhakaram M, Katz M L, Ortwerth B J, Glycation-Mediated Crosslinking Between α-Crystallin and MP26 in Intact Lens Membranes. Mech Age Dev. 91:65-78, 1996
  56. Katz M L, Gao C, Vitamin A Incorporation into Lipofuscin-like Inclusions in the Retinal Pigment Epithelium. Mech Age Dev. 84:29-38, 1995.
  57. Katz M L, Gao C, Tompkins J A, Bronson R T, Chin D T, Mitochondrial ATP Synthase Subunit C Stored in Hereditary Ceroid-Lipofuscinosis Contains Trimethyllysine. Biochem J. 310:887-892, 1995.
  58. Katz M L, Siakotos A N, Canine Hereditary Ceroid-Lipofuscinosis: Evidence for a Defect in the Carnitine Biosynthetic Pathway. Am J Med Genetics 57:266-271, 1995.
  59. Katz M L, Christianson J S, Gao C, Handelman G J, Iron-Induced Fluorescence in the Retina: Dependence on Vitamin A. Invest Ophthalmol Vis Sci. 35:3613-3624, 1994. (http://www.iovs.org/cgi.reprint/35/10/3613.pdf)
  60. Katz M L, Christianson J S, Norbury N E, Gao C, Siakotos A N, Koppang N, Lysine Methylation of Mmitochondrial ATP Synthase Subunit c Stored in Tissues of Dogs with Hereditary Ceroid-Lipofuscinosis. J Biol Chem. 269:9906-9911, 1994.
  61. Katz M L, White H A, Gao C, Roth G S, Knapka J J, Ingram D K, Dietary Restriction Slows Age-Related Accumulation of Lipofuscin in the Retinal Pigment Epithelium. Invest Ophthalmol Vis Sci. 34:3297-3302, 1993. (http://www.iovs.org/cgi/reprint/34/12/3297.pdf)
  62. Katz M L, Stientjes H J, Gao C, Christianson J S, Iron-Induced Accumulation of Lipofuscin-like Fluorescent Pigment in the Retinal Pigment Epithelium. Invest Ophthalmol Vis Sci. 34:3161-3171, 1993. (http://www.iovs.org/cgi.reprint/34/11/3161/pdf)
  63. Katz M L, Gao C, Stientjes H J, Regulation of the Interphotoreceptor Retinoid-Binding Protein Content of the Retina by Vitamin A. Exp Eye Res. 57:393-401, 1993.
  64. Katz M L, Hereditary Ceroid-Lipofuscinosis: Methylated Amino Acids in Storage Body Proteins. J Inherit Metab Dis. 16:305-307, 1993.
  65. Katz M L, Chen D, Stientjes H J, Stark WS, Photoreceptor Recovery in Retinoid-Deprived Rats After Vitamin A Replenishment. Exp Eye Res. 56:671-682, 1993.
  66. Katz M L, Stientjes H J, Gao C, Norberg M, Bright Environmental Light Accelerates Rhodopsin Depletion in Retinoid-Deprived Rats. Invest Ophthalmol Vis Sci. 34:2000-2008, 1993.
  67. Katz M L, Age-Related Alterations in the Retina. In: Lutjen-Drecoll E, ed. Basic Aspects of Glaucoma Research III. Stuttgart: F.K. Schattauer Verlag, pp. 133-152, 1993.
  68. Katz M L, Norberg M, Stientjes H J, Reduced Phagosomal Content of the Retinal Pigment Epithelium in Response to Retinoid Deprivation. Invest Ophthalmol Vis Sci. 33:2612-2618, 1992.
  69. Rodrigues M, Katz M L, Fishman G, Biochemical and Histopathological Changes in Best's Vitelliform Macular Dystrophy. Ophthalmic Practice 10:83-85, 1992.
  70. Katz M L, Gerhardt K O, Methylated Lysine in Storage Body Potein of Sheep with Hereditary Ceroid-Lipofuscinosis. Biochim Biophys Acta. 1138:97-108, 1992.
  71. Katz M L, Norberg M, Influence of Dietary Vitamin A on Autofluorescence of Leupeptin-Induced Inclusions in the Retinal Pigment Epithelium. Exp Eye Res. 54:239-246, 1992.
  72. Eldred G E, Katz M L, The Lipid Peroxidation Theory of Lipofuscinogenesis Cannot Yet Be Confirmed. Free Radical Biol Med. 10:445-447, 1991.
  73. Katz M L, Kutryb M J, Norberg M, Gao C, White R M, Stark W S, Maintenance of Opsin Density in Photoreceptor Outer Segments of Retinoid-Deprived Rats. Invest Ophthalmol Vis Sci. 32:1968-1980, 1991.
  74. Katz M L, Rodrigues M, Juvenile Ceroid-Lipofuscinosis: Evidence for Methylated Lysine in Neural Storage Body Protein. Am J Pathol. 138:323-332, 1991.
  75. Katz M L, Gerhardt K O, Storage Protein in Hereditary Ceroid-Lipofuscinosis Contains S-Methylated Methionine. Mech Age Dev. 53:277-289, 1990.
  76. Katz M L, Incomplete Proteolysis May Contribute to Lipofuscin Accumulation in the Retinal Pigment Epithelium. Adv Exp Med Biol. 266:109-118, 1990.
  77. Katz M L, Shanker M J, Development of Lipofuscin-Like Fluorescence in the Retinal Pigment Epithelium in Response to Protease Inhibitor Treatment. Mech Age Dev. 49:23-40, 1989.
  78. Eldred G E, Katz M L, The Autofluorescent Products of Lipid Peroxidation May Not Be Lpofuscin-Like. Free Radical Biol Med. 7:157-163, 1989.
  79. Katz M L, Eldred G E, Retinal Light Damage Reduces Autofluorescent Pigment Deposition in the Retinal Pigment Epithelium. Invest Ophthalmol Vis Sci. 30:37-43, 1989.
  80. Katz M L, Eldred GE, Failure of Vitamin E to Protect the Retina Against Damage Resulting from Bright Cyclic Light Exposure. Invest Ophthalmol Vis Sci. 30:29-36, 1989.
  81. Eldred G E, Katz M L, Fluorophores of the Human Retinal Pigment Epithelium: Separation and Spectral Characterization. Exp Eye Res. 47:71-86, 1988.
  82. Katz M L, Eldred G E, Siakotos A N, Koppang N, Characterization of Disease-Specific Brain Fluorophores in Ceroid-Lipofuscinosis. Am J Med Genetics Suppl. 5:253-264, 1988.
  83. Katz M L, Drea C M, Robison W G Jr, Age-Related Alterations in Vitamin A Metabolism in the Rat Retina. Exp Eye Res. 44:939-949, 1987.
  84. Katz M L, Robison W G Jr, Light and Aging Effects on Vitamin E in the Retina and Retinal Pigment Epithelium. Vis Res. 27:1875-1879, 1987.
  85. Katz M L, Eldred G E, Robison W G Jr, Lipofuscin Autofluorescence: Evidence for Vitamin A Involvement in the Retina. Mech Age Dev. 39:81-90, 1987.
  86. Katz M L, Drea C M, Robison W G Jr, Dietary Vitamins A and E Influence Retinyl Ester Content and Composition in the Retinal Pigment Epithelium. Biochim Biophys Acta. 924:432-441, 1987.
  87. Katz M L, Drea C M, Eldred G E, Hess H H, Robison W G Jr, Influence of Early Photoreceptor Degeneration on Lipofuscin in the Retinal Pigment Epithelium. Exp Eye Res. 43:561-573, 1986.
  88. Katz M L, Drea C M, Robison W G Jr, Relationship Between Dietary Retinol and Lipofuscin in the Retinal Pigment Epithelium. Mech Age Dev. 35:291-305, 1986.
  89. Katz M L, Robison W G Jr, Evidence of Cell Loss from the Retina During Senescence. Exp Eye Res. 42:293-304, 1986.
  90. Nagata M, Katz M L, Robison W G Jr, Age-Related Thickening of Retinal Capillary Basement Membranes. Invest Ophthalmol Vis Sci. 27:437-440, 1986.
  91. Katz M L, Groome A B, Robison W G Jr, Localization of Lipofuscin in the Duodenums of Vitamin E-Deficient Rats. J Nutr. 115:1355-1365, 1985.
  92. Katz M L, Robison W G Jr, Senescence and the Retinal Pigment Epithelium: Alterations in Basal Plasma Membrane Morphology. Mech Age Dev. 30:99-105, 1985.
  93. Katz M L, Robison W G Jr, Herrmann R K, Groome A B, Bieri J G, Lipofuscin Accumulation Resulting from Senescence and Vitamin E Deficiency: Spectral Properties and Tissue Distribution. Mech Age Dev. 25:149-159, 1984.
  94. Katz M L, Robison WG Jr, Age-Related Changes in the Retinal Pigment Epithelium of Pigmented Rats. Exp Eye Res. 38:137-151, 1984.
  95. Katz M L, Robison W G Jr, Lipofuscin Response to the "Aging-Reversal" Drug Centrophenoxine in Rat Retinal Pigment Epithelium and Frontal Cortex. J Gerontol. 38:525-531, 1983.
  96. Katz M L, Parker K R, Handelman G J, Farnsworth C C, Dratz E A, Structural and Biochemical Effects of Antioxidant Nutrient Deficiency on the Rat Retina and Retinal Pigment Epithelium. Ann NY Acad Sci. 393:196-197, 1982.
  97. Katz M L, Parker K R, Handelman G J, Bramel T L, Dratz E A, Effects of Antioxidant Nutrient Deficiency on the Retina and Retinal Pigment Epithelium of Albino Rats: A Light and Electron Microscopic Study. Exp Eye Res. 34:339-369, 1982.
  98. Stone W L, Katz M L, Lurie M, Marmor M F, Dratz E A, Effects of Vitamin E and Selenium Deficiency on Light Damage to the Rat Retina. Photochem Photobiol. 29:725-730, 1979.
  99. Katz M L, Stone W L, Dratz E A, Fluorescent Pigment Accumulation in Retinal Pigment Epithelium of Antioxidant Deficient Rats. Invest Ophthalmol Vis Sci. 17:1049-1058, 1978.

Other Publications

  1. Katz M L, Johnson G S, Drögemüller C, Canine Neuronal Ceroid Lipofuscinoses. In: Mole S E, Lake B D, Goebel H H, eds. The Neuronal Ceroid Lipofuscinoses (Batten Disease), 2nd Ed. London: IOS Press, In press, 2008.
  2. Narfström K, Katz M L, Bragadottir R, Ford M M, Redmond T M, Lai M J T, Brankov M, Barnett N L, Moore S R, Stoddart C W, Martin-Iverson M T, Rakoczy P E, Partial Recovery of Retinal Function in RPE65-/- Mice and Dogs Following rAAV-Mediated Gene Therapy. In: Redberry G W, ed. Trends in Gene Therapy Research. Hauppauge, NY: Nova Science Publishers, pp. 129-145, 2005.
  3. Feeney-Burns L, Katz M L, Retinal Pigment Epithelium. In: Tasman W, Jaeger E, eds. Duane's Foundations of Clinical Ophthalmology. Philadelphia: JB Lippincott, Chapter 21, pp. 1-20, 1992.
  4. Katz M L, Robison W G J, Senescent Alterations in the Retina and Retinal Pigment Epithelium: Evidence for Mechanisms Based on Nutritional Studies. In: Armstrong D, Marmor M F, Ordy J M, eds. The Effects of Aging and Environment on Vision. New York: Plenum Press, pp. 195-208, 1991.
  5. Katz M L, Robison W G Jr, Consequences of Impaired Antioxidant Protection of the Retina. In: Miquel J, Quintanilha A, Weber H, eds. Handbook of Free Radicals and Antioxidants in Biomedicine, Volume II, Boca Raton, Fla: CRC Press, Inc., pp. 289-301, 1989.
  6. Eldred G E, Katz M L, Possible Mechanism for Lipofuscinogenesis in the Retinal Pigment Epithelium and Other Tissues. In: Zs.-Nagy, ed. Lipofuscin 1987: State of the Art. Amsterdam: Elsevier Science Publishers, pp. 185-211, 1988.
  7. Katz M L, Robison W G Jr, Autoxidative Damage to the Retina: Potential Role in Retinopathy of Prematurity. In: Flynn J T, Phelps D L, eds. Retinopathy of Prematurity: Problem and Challenge. New York: Alan R. Liss, Inc., pp. 237-248, 1988.
  8. Katz M L, Robison W G Jr, Drea C M, Factors Influencing Lipofuscin Accumulation in the Retinal Pigment Epithelium of the Eye. In: Totaro E A, Glees P, Pisanti F A, eds. Advances in Age Pigments Research. Oxford: Pergamon Press, pp. 111-131, 1987.
  9. Robison W G Jr, Katz M L, Vitamin A and Lipofuscin. In: Sheffield J B, Hilfer S R, eds. Cell and Developmental Biology of the Eye, Vol. 6: The Microenvironment and Vision. New York: Springer-Verlag, pp. 95-122, 1987.
  10. Katz M L, Robison W G Jr, Nutritional Influences on Autoxidation, Lipofuscin Accumulation, and Aging. In: Johnson J E, Walford R, Harmon D, Miquel J, eds. Free Radicals, Aging, and Degenerative Diseases. New York: Alan R. Liss, Inc., pp. 221-259, 1986.
  11. Katz M L, Robison W G Jr, Dratz E A, Potential Role of Autoxidation in Age Changes of the Retina and Retinal Pigment Epithelium of the Eye. In: Armstrong D, Sohal R S, Cutler R G, Slater T F, eds. Free Radicals in Molecular Biology, Aging, and Disease. New York; Raven Press, pp. 163-180, 1984.
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