DONALD ZACK, M.D.
Medical Practice at Wolfe St, Baltimore, MD

2004018, Sep 16, 2004

Jul 14, 2003

10/618084

Donald Zack - Baltimore MD, US
Abigail Hackam - Baltimore MD, US

The Johns Hopkins University - Baltimore MD

A61K039/395, C12N005/08

424/143100, 435/368000

The retinal degeneration (rd1) mutant mouse exhibits rapid rod photoreceptor degeneration caused by a mutation in the rod photoreceptor-specific gene cGMP phosphodiesterase (PDE). One intriguing aspect of the rd1 phenotype is a secondary wave of cone photoreceptor death that follows loss of rods. In this study, we investigated gene expression changes associated with the progression of photoreceptor degeneration in rdmice using a custom retina microarray. The microarray contains 5,376 DNA fragments that correspond to mouse genes known or postulated to be involved in normal retinal function, development, or disease. Gene expression in rd1 retina was compared with age-matched wild-type controls at three time-points corresponding to critical stages in retina degeneration: peak of rod degeneration, early in cone degeneration and during cone degeneration. Statistical significance analyses demonstrated that approximately 3% of the genes on the microarray were differentially expressed, including known genes and genes that had not been previously implicated in degeneration. Interestingly, there was less overlap in the genes that were upregulated at each stage of degeneration, suggesting the involvement of distinct molecular pathways. Genes involved in transport, signalling and cytoskeleton were differentially expressed during rod degeneration whereas genes involved in growth and proliferation, oxidative stress and protein modification were increased prior to and during cone degeneration. These results provide clues to underlying molecular processes occurring during photoreceptor degeneration, and provide direction for future cell-based studies.

2004008, Apr 29, 2004

Jul 14, 2003

10/617888

Donald Zack - Baltimore MD, US
Harry Quigley - Baltimore MD, US

The Johns Hopkins University - Baltimore MD

A61K039/395

424/146100, 424/145100

The optic nerve axotomy model in mouse exhibits rapid changes in gene expression. Genes identified by microarray analysis as differentially expressed or modulated in this model, can be used diagnostically, therapeutically, and in drug discovery. These results provide clues to underlying molecular processes occurring during optic nerve degeneration, and provide direction for future cell-based studies.

2004008, May 6, 2004

Jul 14, 2003

10/617885

Donald Zack - Baltimore MD, US
Masaaki Kageyama - Osaka, JP

The Johns Hopkins University - Baltimore MD

A61K039/395

424/146100

Neuronal cell death, as modeled by removal of serum or NGF from growth medium, is characterized by many changes in gene expression. Gene expression was compared before and after withdrawal of serum or NGF. These results provide clues to underlying molecular processes occurring during neuronal and photoreceptor degeneration, and provide direction for future cell-based studies.

2013021, Aug 22, 2013

Mar 23, 2011

13/636415

Donald J. Zack - Baltimore MD, US
Thomas Bannister - Palm Beach Gardens FL, US
Tomas Vojkovsky - Palm Beach Gardens FL, US
Zhiyong Yang - Baltimore MD, US
Cynthia Berlinicke - Baltimore MD, US

THE SCRIPPS RESEARCH INSTITUTE - La Jolla CA
THE JOHNS HOPKINS UNIVERSITY - Baltimore MD

C07D 209/34, A61K 31/55, A61K 31/454, C07D 403/06, A61K 31/496, C07D 453/02, A61K 31/439, A61K 45/06, A61K 31/404, A61K 31/5377

51421708, 548455, 514414, 540602, 546201, 514323, 5142352, 544144, 51425409, 544373, 546133, 514305, 435375, 548468

Compounds, compositions, kits and methods for treating conditions related to neurodegeneration or ocular disease, are disclosed.

2009021, Aug 27, 2009

Apr 24, 2006

11/918987

John Barnwell Kerrison - Towson SC, US
Donald J. Zack - Baltimore MD, US

The Johns Hopkins University - Baltimore MD

A61K 31/5377, C12Q 1/68, G01N 33/53, C12N 5/02, A61K 31/497, A61K 31/445, C07D 413/14, C07D 239/02, C07D 211/68

5142322, 435 6, 435 72, 435375, 51425401, 514315, 544107, 544297, 546244

Neuroprotective compounds for treating optic neuropathies and screening methods for identifying neuroprotective compounds.

2011017, Jul 14, 2011

Aug 8, 2009

13/058171

Donald Jeffrey Zack - Baltimore MD, US
Zhiyong Yang - Baltimore MD, US
Cynthia Berlinicke - Baltimore MD, US
Harry Quigley - Baltimore MD, US

THE JOHNS HOPKINS UNIVERSITY - Baltimore MD

A61K 31/404, A61P 25/28, A61P 27/06, A61K 31/553, C07D 403/06, A61K 31/496, C07D 403/14, C07D 498/22, C12N 5/079

51421108, 514414, 548468, 51425409, 544373, 540545, 548455, 435375

Compounds, compositions, kits and methods for treating conditions related to neurodegeneration or ocular disease, are disclosed.