[Neuroscience] Re: Carotenoid Transport into the RPE
(by johnh from goawayplease.com)
Mon Dec 10 02:52:39 EST 2007
Have read this one. They key phrase is
Responding eyes had significantly lower baseline MP concentration than did
nonresponding eyes. Central vision was unchanged after the period of
Once the photoreceptors are gone there aint no turning back, hence visual
recovery is rare. Where it does occur it probably relates to neurons that
are on the way out hence not working probably and subsequently saved by the
On a positive note though, there are some very promising clinical trials on
gene and stem cell therapies. Neurons are clever little bastards, just place
ém in the right environment and they often morph into the right form and
function. Amazing stuff. Those odd Aussies have already created cochlear
implants that are getting better by the year and there is no intrinsic
reason why the same won't happen with vision. In a sense it already has,
artificial retinas have been implanted in humans and are, albeit in a very
limited sense, functional.
"Don W" <dwilgus from prodigy.net> wrote in message
news:V%27j.23597$4V6.219 from newssvr14.news.prodigy.net...
> 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
> 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
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