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[Neuroscience] Re: Carotenoid Transport into the RPE

Don W via neur-sci%40net.bio.net (by dwilgus from prodigy.net)
Sun Dec 9 23:11:33 EST 2007


John,

  I had thought that since Stargardt's and ARMD could both benefit from 
anything that would increase the macular pigment (MP), that is would be nice 
to measure how well taking lutein/zeaxantan affects the macula.  First 
measure the improvement (increase) and then see how well this affects 
acuity.  I had wondered before if increases in MP would directly affect 
acuity.  This paper answers this question somewhat.  This paper was 
presented at ARVO 2006.  Did not like the comment that central vision was 
not changed.  Oh and MP density correlated with OCT retinal thickness, as 
mentioned in the original ARVO abstract.

  Have other comments, but just found original abstract in my Misc file.

Don W.


*****



Investigative Ophthalmology and Visual Science. 2007;48:1319-1329.)
© 2007 by The Association for Research in Vision and Ophthalmology, Inc.
 Articles by Jacobson, S. G.

Macular Pigment and Lutein Supplementation in ABCA4-Associated Retinal 
Degenerations
Tomas S. Aleman,1 Artur V. Cideciyan,1 Elizabeth A. M. Windsor,1 Sharon B. 
Schwartz,1 Malgorzata Swider,1 John D. Chico,1 Alexander Sumaroka,1 
Alexander Y. Pantelyat,1 Keith G. Duncan,2 Leigh M. Gardner,1 Jessica M. 
Emmons,1 Janet D. Steinberg,1 Edwin M. Stone,3 and Samuel G. Jacobson1
1From the Scheie Eye Institute, Department of Ophthalmology, University of 
Pennsylvania, Philadelphia, Pennsylvania; the 2Department of Ophthalmology, 
University of California, San Francisco, California; and the 3Department of 
Ophthalmology, University of Iowa Carver College of Medicine, Iowa City, 
Iowa.


PURPOSE. To determine macular pigment (MP) optical density (OD) in patients 
with ABCA4-associated retinal degenerations (ABCA4-RD) and the response of 
MP and vision to supplementation with lutein.

METHODS. Patients with Stargardt disease or cone-rod dystrophy and known or 
suspected disease-causing mutations in the ABCA4 gene were included. All 
patients had foveal fixation. MPOD profiles were measured with 
heterochromatic flicker photometry. Serum carotenoids, visual acuity, foveal 
sensitivity, and retinal thickness were quantified. Changes in MPOD and 
central vision were determined in a subset of patients receiving oral 
supplementation with lutein for 6 months.

RESULTS. MPOD in patients ranged from normal to markedly abnormal. As a 
group, patients with ABCA4-RD had reduced foveal MPOD, and there was a 
strong correlation with retinal thickness. Average foveal tissue 
concentration of MP, estimated by dividing MPOD by retinal thickness, was 
normal in patients, whereas serum concentration of lutein and zeaxanthin was 
significantly lower than normal. After oral lutein supplementation for 6 
months, 91% of the patients showed significant increases in serum lutein, 
and 63% of the patients' eyes showed a significant augmentation in MPOD. The 
retinal responders tended to be female and to have lower serum lutein and 
zeaxanthin, lower MPOD, and greater retinal thickness at baseline. 
Responding eyes had significantly lower baseline MP concentration than did 
nonresponding eyes. Central vision was unchanged after the period of 
supplementation.

CONCLUSIONS. MP is strongly affected by the stage of ABCA4 disease leading 
to abnormal foveal architecture. MP could be augmented by supplemental 
lutein in some patients. There was no change in central vision after 6 
months of lutein supplementation. Long-term influences of this supplement on 
the natural history of these macular degenerations require further study




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