SightSight The Schepens EyeResearch Institute

Stolen SightWhy Nana Can’t

Recognize JohnnyPage 3

ingsWinter 2003

Age-related Macular Degeneration

2

e Americans live in anextraordinary time and place: a highstandard of living, combined with asuperb health-care delivery system haslengthened human life well beyondthe expectations of only a generationago. My father made few plans for hisretirement because he fully expecteddeath to intervene within a few yearsof his 65th birthday. To his surprise(and to my great thankfulness), helived to the age of 88; my mother, five years his junior, lived to the ageof 87. During the last two decades oftheir full lives, my parents experiencedthe diseases associated with aging: inmy father’s case, arteriosclerotic heartdisease and prostatic cancer; for mymother, Alzheimer’s disease and age-related maculardegeneration.

It is incumbentupon those of us whoconduct biomedicalresearch, as well asthose who supportthis type of research in the spirit of phi-lanthropy, to direct our attention tothe diseases that rob our senior citi-zens of happiness and comfort as lifeslowly ebbs. Since not all individualsof advanced age come to suffer fromthese so-called age-related diseases,the problem does not appear to be theaging process itself. Therefore, it isimportant to distinguish aging as abiologic phenomenon from age-relat-ed diseases as pathologic processes. A major goal of The Schepens EyeResearch Institute is to find the causesand develop preventions and cures for age-related diseases of the eye.Whereas macular degeneration is themost widely known and feared eyedisease of the over-65 set, it mustshare its notoriety with diabetic

retinopathy,glaucoma, anddry eye syn-drome as theso-called “fourhorsemen ofage-relatedvision loss.”Our research efforts extend to each of these four diseases.

Everyone is aware of the fact thatthe American population is “aging.”This means that with each passingyear a progressively larger proportionof the population is older than 65years. At present, approximately 12.7 percent of Americans fit into this category. By the year 2030, thisnumber will grow to 20 percent! As

an example, there are 3.6 million Americans who now suffer from age-related macular degenera-tion. By the year 2030,this number will swell to 6.3 million. While theword epidemic is toohistrionic to use in this

context, the projected increasedprevalence of age-related eye diseasesin America (and in other developedcountries) in the next decades repre-sents a crisis unfolding.

As the leading eye research organi-zation in America, The Schepens EyeResearch Institute is working on sev-eral fronts to meet, and if possible,prevent, this crisis. More than a yearago, the Institute created the Centerfor Research on the Aging Eye, a mul-tidisciplinary effort by many of ourscientists who are working collabora-tively to solve the most vexing prob-lems. The Institute houses the JuvenileDiabetes Foundation’s first DiabeticRetinopathy Research Center with the goal of preventing the earliest

From the President

Board of TrusteesJ. H. Walton, Jr., Chairmanof the BoardCharles L. Schepens, M.D.,Founder and ChairmanEmeritus

William F. AikmanDeWalt H. Ankeny, Jr.George D. Bell, Jr.Dean Bok, Ph.D.Kennett F. BurnesJennifer F. CabotCharles S. de GunzburgAlice R. Dietrich Harold L. Emerson Kenneth M. FischerRobert L. GableGerard D. Goldstein Richard Harte, Jr.Donald R. Korb, O.D.David T. LawrenceSimmons Lessell, M.D.Renée Manger J. Wallace McMeel, M.D.Patricia PatricelliElio Raviola, M.D., Ph.D.E. Richard RothmundCharles L. Schepens, M.D.Eleanor G. Shore, M.D.Sherman H. StarrGlenn P. StrehleDennis R. TourseA. Raymond TyeKathryn C. Vecellio Theodore N. VossJ. H. Walton, Jr.Babbette Wolff

Honorary TrusteesMarie H. AnkenyEvelyn M. AxelrodCharles J. CellaMichael J. CrimiJ. Edward Lundy

Sightings is produced by theOffice of Development,Melanie Saunders, Editor

For more information or for extra copies, please call(617) 912-2666.

W

“More than a year ago, the

Institute created the Center

for Research on the Aging Eye,

a multidisciplinary effort by

many of our scientists who are

working collaboratively to solve

the most vexing problems.”

(continued on page 9)Cover photo courtesy of the National Eye Institute

3

Why Nana Can’t Recognize Johnny

Stolen Sight

“I will be standing there andsomeone approaches me, andno matter how well I knowthem, until they come up closeto me, I really can’t tell whothey are. This is true of mychildren, my grandchildren, mygreat grandchildren, and mybest friends,” says 84-year-oldIna Ward, grandmother ofseven, great grandmother ofsix, and victim of age-relatedmacular degeneration (AMD).

Recognizing the people weknow and love at first glance issomething most ofus count on andtake for granteduntil that abilitybegins to dissolvewith fading vision.“In many ways thisis the most difficultpart of having mac-ular degeneration,”says Ward. “It canbe really terribleand depressing for me and I amsure disconcerting for my fami-ly and friends, especially mygreat grandchildren who arestill pretty little and don’t reallyunderstand.”

Depression is a commoncompanion of AMD, alongwith frustration and embarrass-ment. And, it is not just loss of face recognition skills thatcontributes to this malaise.Reading, driving, and otherskills that impart a sense ofcompetency and independence

are also in jeopardyfrom a disease thatslowly robs the eye ofwhat most people feelvision is all about,according to KameranLashkari, M.D., assis-tant clinical scientistat The Schepens EyeResearch Institute.

When asked whyface recognition is sodifficult for AMDpatients, Schepensexperts describe what it is like

for the person withAMD. They say, “It is like looking at a face through a piece of gauze,” or “It is like seeing someonethrough a Swiss cheese-like pattern,” or “It islike watching a televi-sion picture that has nocontrast.” But howeverit is described, the facts

for sufferers like Ina Ward arethe same.

AMD is a disease that slowlyand irreversibly destroys someof the most precious cells in thehuman eye and, indeed, thehuman body: the light-sensitive(photoreceptor) cells of themacula. The macula is the tinycenter of the retina which is thefilm of neural (nerve) tissue atthe back of the eye that cap-tures images from the outsideand transmits them through theoptic nerve to the brain. The

macula is the part of the eyeresponsible for detail, color,and the sharp focus needed fordriving, reading, and recog-nizing faces.

“Because AMD can be dev-astating to a person’s life andlifestyle, early detection, futureprevention if possible, andaccess to rehabilitation areessential,” says Lashkari, whohas seen hundreds of peoplewith AMD in his practice.

The Schepens Eye ResearchInstitute scientists are exploringall aspects of this sight-stealingdisease to help detect it earlier,mitigate its impact, and ulti-mately find a way to cure it.

About AMDAMD is the leading cause of

low vision and central blind-ness in Americans over 65.Nearly 10 percent of the popu-lation over age 52 has AMDand up to 33 percent of those

Kameran Lashkari, M.D.,Assistant ClinicalScientist

(continued on next page)

4

older than 75 are afflicted.With the aging of the generalpopulation, by the year 2030, 6 million Americans will beafflicted. Risk factors for AMDinclude smoking, high fat diets,diets low in antioxidants, beingfemale and Caucasian, over-exposure to sunlight, and apossible genetic predisposition.

Although there are two formsof AMD, dry and wet, manyexperts would argue that theunderlying basis for these twodiseases is the same. In drymacular degeneration, the cellsof the macula slowly begin toatrophy and die over a periodof years. Wet AMD developswhen new, abnormal bloodvessels start to grow in a layerof vascular tissue beneath theretina called the choroid mem-brane. These tiny blood vesselsbreak through tissue calledBruch’s membrane and bleed,and in the process, kill, macu-lar cells—causing loss of cen-tral sharp vision within days orweeks.

In both cases, patients initial-ly complain of visual distor-tions and unexplained blurredvision. Because AMD progress-es slowly in the early stages, bythe time a patient notices thesechanges the disease is alreadyfairly advanced. On visualexamination, a physician willsee yellow spots under theretina, known as drusens,which seem to be a precursorof the disease.

At this point, there are notreatments for dry maculardegeneration. The purpose ofexisting treatments, which aredesigned only for wet AMD,

has been to stop thebleeding by destroy-ing the blood vesselsbefore they destroythe photoreceptors.Until recently, laserphotocoagulation has been the mostcommon treatment.Now photodynamictherapy (PDT) is thetreatment of choicebecause it is morefocused and destroysfewer healthy cells than theearlier treatment. In PDT, the drug selectively enters the vacuolar cells within themembrane and destroys themwithout directly damaging theretina. Neither procedure is acure. PDT generally requiresrepetition because these bloodvessels have a tendency torecur.

“The limited options are verydisheartening to patients likeIna Ward,” says Lashkari.“They feel that they have losttotal control over what is hap-pening to their eyes and totheir lives because of AMD.”

Giving patients back a sense of control overtheir vision and theirlives is a major goal ofthe research efforts at TheSchepens Eye ResearchInstitute.

Learning more about the cause

“One of the possiblecauses of this mess calledAMD is a chemical known aslipofuscin, which is found inlarge quantities in the eyes

of older people and in patientswith some other macular dys-trophies,” says François Delori,Ph.D., senior scientist at TheSchepens Eye Research Insti-tute. Delori is determined tolearn whether high levels oflipofuscin play a role in thedevelopment of AMD.

Found in the retina pigmentepithelium or RPE (a layer oftissue under the retina attachedto the blood supply), lipofuscinis a waste product of a processthat daily renews the photore-ceptor cells in the macula. After a day of light exposure, thephotoreceptor cells lose their

outer tips anddevelop new layers.The RPE, whichpromotes the shed-ding of the oldmembranes, alsodigests them anddelivers the wasteproducts to theblood stream to be carried away.The tiny remaining

portion of those waste productsis lipofuscin. “Although wedon’t know if lipofuscin isfound in babies eyes, it does

François Delori, Ph.D.,Senior Scientist

Stolen Sight (continued from page 3)

Age-related Macular Degeneration

5

exist in teenagers and we knowit accumulates throughout lifeand reaches high levels in oldage,” he says.

Delori believes that conges-tion caused by large quantitiesof lipofuscin might destabilizethe photoreceptor cells andprevent their normal activity.Understanding how lipofuscinin different levels contributes tothe development of AMD andother retinal diseases couldultimately lead to a new diag-nostic tool for early detection,notes Delori, who is currentlyinvolved in a twin study tolearn if levels of lipofuscin aregenetically determined. “It isanother piece of the AMDpuzzle,” he says.

While Delori’s work may notchange Ina Ward’s prognosis, itcould help diagnose the poten-tial for AMD in her offspring.

Prevention is the keyMax Snodderly, Ph.D., senior

scientist at The Schepens EyeResearch Institute, believes thatnutrition may be a useful toolfor retarding the process thatleads to AMD. “I really wantto know what is going on earlyin the process,” he says. “If wecan figure that out, we caneliminate this disease.”

Snodderly is gathering dataon the role that carotenoid pig-ments play in the macula, andwhether supplementing them in the diet can help delay orprevent the onset of AMD.Although Snodderly has beeninvolved in studies of othernutritional factors, he is partic-ularly interested in lutein and

zeaxanthin,which are thepigments inthe macula.The theory isthat these pig-ments protectthe maculafrom lightdamage just as they protectplants during photosynthesis.Previous studies have alreadyshown that levels of thesechemicals are low in the retinasof AMD patients and in smok-ers. There is also suggestiveevidence that women absorblutein less readily than men dofrom the diet.

According to Snodderly,carotenoid supplements havehad a lot of promotion in thepress, and many people arealready taking them. However,he believes long-term, large-scale studies are needed toconfirm the effectiveness ofsupplementing with thesechemicals.

Snodderly’s research mayhelp to stabilize Ina Ward’s dis-ease, but more importantly, itmay help prevent it in her chil-dren or grandchildren.

A passion for readingFor Elisabeth Fine, Ph.D.,

assistant scientist at TheSchepens Eye Research Insti-tute, reading is a passion inmore ways than one. She lovesto read, and she believes losingthat ability would be the worstpart of AMD. Learning how tohelp people regain that abilityis her passion and her work.

To help her shed light onAMD’s impact on reading,Fine uses an optical imagestabilizer to put people withnormal vision under condi-tions that simulate some ofthe visual impact of AMD. “Ican give them the central fieldloss common in AMD andtake it away and see how itchanges their ability to read.”

With this technique, she canask questions and make com-parisons she cannot make withAMD patients. For example,she can compare reading withlarge and small blind spots, orchange the position of the blindspot. By introducing a simulat-ed scotoma(blind spot)into a per-son’s visualfield, Fine canlook at howthis changesreading timeand the eyemovementsmade to read.

Fine can also look at whatpart of the retina each personuses as a substitute for themissing fovea. People who havecentral field loss often developa “pseudo-fovea,” which is anarea on the retina that they useas a substitute for the missingfovea. The fovea not only hasthe most detailed vision, it isalso the anchor for eye move-ments and for visual attention.“We use both to move our eyesto sample the information inthe visual world,” says Fine,who has a theory that the pseu-

Max Snodderly, Ph.D.,Senior Scientist

(continued on page 14)

Elisabeth Fine, Ph.D.,Assistant Scientist

6

Ask aSchepens Scientist...Schepens Scientist...Born in Chicago, Illinois,

Andrew W. Taylor earned hisbachelor of science in biochem-istry from the University ofWisconsin in 1983. He went onto obtain a master of science inImmunogenetics in 1986 and a Ph.D. in Microbiology andImmunology in 1990 fromOhio State University.

In 1990, Taylor became partof the team at the University of Miami School of Medicine,headed by J. Wayne Streilein,Ph.D., now president of The Schepens Eye ResearchInstitute. There Taylor discov-ered several immunosuppressivefactors in the eye. He joinedThe Schepens Eye Research In-stitute in 1993, where he con-tinues in his commitment tounravel the mystery of the eye’simmune privilege. He is theauthor of 37 publications inImmunology, Visual Science,and Neuroimmunology.

Q: I have heard that somemolecules in the eye may helpprevent inflammation and mayaffect autoimmune diseases inthe eye and other parts of thebody. Can you enlighten me?

A: To answer your question, I first need to describe the waythe immune system works in the eye.

Because it is extremely intri-cate, delicate, and so vital tosurvival, the eye has evolved aspecial way of handling immu-nity to prevent inflammation inresponse to foreign invaderssuch as bacteria, viruses, andother harmful substances. In the scientific community, we

say that the eye is “immuneprivileged.”

At The Schepens Eye ResearchInstitute, my laboratory is partof a team of other scientists and laboratories determined toincrease our understanding ofthis “privileged” state and howit might be harnessed to preventinflammation not only in theeye but in other parts of thebody as well.

In most other tissues of thebody, the immune response toforeign invaders involves therallying of several cells and sub-stances to fight off the threat.With T cells as the ringleadersof this process, the defensiveresponse eventually causesinflammation, characterized byredness and swelling. As theinvader is defeated, the inflam-mation gradually subsides andthe tissue heals.

But in the eye, inflammationof any kind can cause irrepara-ble damage to its delicate tissuesand thus to vision. So the act ofprotecting itself in the typicalway is devastating to the eye.

Faced with this dilemma, theeye evolved a way to suppressthe inflammatory immuneresponse. The eye’s specialimmune suppressive propertiesare something that scientistshave known about for 150years, and are the explanationfor the success of corneal trans-plants. Corneal transplants havea very low rate of rejection andthe highest success rate for anytransplanted tissue.

Although there are manyunknown factors involved inthis immune suppression, wehave begun to find some impor-tant clues over the past decade.In my laboratory at the Institute,we have discovered at least oneof the keys to unlocking themystery.

In animal studies supportedby the National Eye Institute,we identified a factor within theaqueous humor of the eye calledalpha-melanocyte stimulatinghormone (alpha-MSH), whichplays an important role in theprocess. This molecule, welearned, blocks the immunesystem from initiating inflam-mation in response to foreignthreats. It does this by causingthe development of regulatory T cells, cells which turn offother T cells that are responsi-ble for the inflammatoryimmune response. Alpha-MSHalso causes T cells to convertinto regulatory T cells. Whenwe learned that the activity ofthis factor is very low in caseswhere the eye becomes inflamed,we knew we were on to some-thing very important.

Andrew W. Taylor, Ph.D.,Associate Scientist at The SchepensEye Research Institute and AssistantProfessor at Harvard Medical School.

(continued on back cover)

7

For nearly a decade, MadelonZimner has been making annualgifts of $100 to The SchepensEye Research Institute in lovingmemory of her late husbandBen. Madelon has a strongdesire to support the Institute’swork so that others may bespared from the devastatingeffects of blindness—a crusadethat she has been on since1985, when Ben Zimner wasrobbed of his sight by maculardegeneration.

“I truly wish I could givemore,” Madelon has frequentlysaid, “but I am living on a fixedincome.”

Speaking to Madelon Zimner,one soon realizes how much sheadored her husband. “Ben wasa wonderful husband and father,”Madelon recalls, “and he wasso handsome ... he looked like a movie star.” It is understand-able therefore that Madelonfeels so strongly about theInstitute’s dynamic researchefforts to cure blindness. At theage of 72, Ben was afflictedwith an aggressive form of mac-ular degeneration that renderedhim legally blind overnight.According to Madelon, “mostpeople, including physicians,are not aware of the devasta-tion that blindness can cause.Ben suffered from clinicaldepression as a result of hissudden blindness and it affectedour entire family. He lost hiswill to live when he lost hissight and that deprived us of

the love and affectionthat we normallyshared.”

Although there was no cure to restore Ben’ssight, the Zimners foundcomfort in the medicalcare they received fromDr. Marc Yoshizumi, anaccomplished ophthal-mologist who had trainedat The Schepens EyeResearch Institute. “Dr.Yoshizumi understoodthe emotional and psy-chological effects of blind-ness and recommendedpsychotherapy to treat Ben’sdepression,” Madelon explains.Heeding Dr. Yoshizumi’s advice,“Ben received counseling fromDr. Rhebe Aquado, a clinicalpsychologist, who helped Bendramatically,” according toMadelon.

Madelon was delighted tolearn that she could make alarger gift than she thoughtpossible to support the Insti-tute’s research by contributingthrough a Charitable GiftAnnuity. It is quite a simplearrangement. In exchange foran irrevocable gift of cash orsecurities, the Institute agrees to pay the donor an annuityeach year for the remainder ofhis or her life. The older the

donor is at the time of the gift,the greater the annuity that theInstitute can pay. In Madelon’scase, the 8 percent annuity pay-ment was far greater than shecould receive from a moneymarket or certificate of deposit,and she was entitled to take asignificant income tax deduc-tion. The tax and financialbenefits of a Charitable GiftAnnuity enabled Madelon toachieve her philanthropicdreams by making a five-figuregift to the Institute in memoryof Ben. As Madelon put it, “Iam not a wealthy woman. Thisis the only way for me to make a gift of this size.”

“I am receiving so muchmore than I am giving,”Madelon commented recently,after seeing the research of Dr. Michael Young, assistantscientist at The Schepens, fea-tured on the PBS program,

The Gift of a Lifetime—in Loving Memory of Ben

Profiles in Philanthropy

(continued on page 14)

“I am not a wealthy woman.This is the only way for me to make a gift of this size.”

Ben and Madelon Zimner

William W lff Society

T H E

I N S T I T U T EAro

und8

The Schepens participated in the National EyeInstitute’s traveling exhibit on low vision—the kickoffevent was held on Monday, June 3 at the CambridgeSideGalleria, Cambridge, MA. The Eye Sight, which providedinformation on low vision in English and Spanish, fea-tured five kiosks with an interactive multimedia touchscreen program, a display of assistive devices, and a listof local low vision resources. The exhibit was free andopen to the public. Congressman Michael Capuano andmembers of the Eye Sight committee kicked off the eventwith a ribbon cutting ceremony.

Traveling exhibit kicks off at the CambridgeSide Galleria

9

New PublicationHighlights Financialand PhilanthropicPlanning

A new publication by The Schepens Eye ResearchInstitute, entitled “Envision,” isbeing sent to many of our long-time friends and donors. Thenewsletter provides informationthat is timely and helpful inplanning for the future. Manyof the Institute’s friends weredelighted to learn about theattractive benefits offered bythe estate, financial, and philan-thropic opportunities featuredin the inaugural issue.

If you are interested in thispublication, send us your nameand address and we will besure to forward a copy to you.Send it to George Constant,The Schepens Eye ResearchInstitute, 20 Staniford St.,Boston, MA 02114, or e-mailconstant@vision.eri.harvard.edu.

This December we will take to the telephones again,reaching out to our loyal supporters to enable our scientistsand researchers to continue their quest to conquer blindingeye disease. With your help, we will reach our goal to sup-port the operational needs of the Institute and ongoingresearch projects. If one of our callers reaches you, pleasebe as generous as you can.

Annual Winter Phonathon

stages of this dreaded compli-cation of diabetes mellitus.Multidisciplinary teams ofresearch workers at theInstitute are working towardtruly innovative treatments for age-related blinding dis-eases through the Minda deGunzburg Research Center for Retinal Transplantation,and through the Ocular GeneTherapy Research Program. In aggregate, these researchefforts represent a full-scaleattack upon the problem.

Yet we are acutely awarethat these diseases are alreadycausing serious vision loss inpeople who are now in theover-65 age group. Until andunless cures and preventionscan be found, it is extremelyimportant that our researchscientists seek strategies thatwill offer—here and now!—relief for people whose visionis already impaired. The lead-ing scientists in the worlddeveloping novel low visionaids are working at theInstitute, and their researchholds great immediate promise.

This issue focuses on age-related macular degeneration

From the President (continued from page 2)

—enumeration of its possiblecauses, improved methods forevaluation of retinal function,current methods of treatment,and the role of nutrition. Ihope that you will find thisissue informative and helpful.

Although a crisis withrespect to preservation of finevision is looming as theAmerican population agesover the next decades, the cri-sis can be avoided. Along withtheir peers at numerous bio-medical research institutionsaround the world, the scien-tists at The Schepens EyeResearch Institute are workinghard to find answers that canbe translated into clinical ben-efit. We are pleased that youhave joined us in this effort—with your encouragement,your support, and yourprayers. Together we can stop the “four horsemen.”

Sincerely,

J. Wayne Streilein, M.D.President

10

Kathryn Colby, M.D., Ph.D.,Director, Joint Clinical ResearchCenter, Massachusetts Eye andEar Infirmary, The SchepensEye Research Institute, wasborn and raised in New Jersey,and received her B.A. at JohnsHopkins Universityin 1981, a Ph.D. inNeurobiology fromBrown University in1986, and her M.D.from the Universityof Maryland MedicalSchool in 1992. Fol-lowing an internshipin internal medicineat Mercy MedicalCenter in Baltimore,she went on to com-plete her ophthal-mology residency atMassachusetts Eye and EarInfirmary (MEEI) in 1996.

Colby is now a cornealspecialist and a full-time staffmember at MEEI. In 1998 shebecame the founding director of the Joint Clinical ResearchCenter and an investigator atThe Schepens Eye ResearchInstitute. Her special interestsare corneal endothelial dystro-phies and ocular surface tumors.

Colby currently lives in Win-chester, Massachusetts, with hertwo daughters.

Question: My doctor keepstelling me that I should havecorneal transplantation. Theidea scares me. Should I beworried?

Answer: You should alwaysthink carefully about any surgi-cal procedure, but the facts

about corneal transplantationmay help to ease your fears andhelp you make an educateddecision.

Approximately 35,000 peoplea year undergo corneal trans-plantation in the United States,

and 95 percent havesuccessful results. Theprocedure is so wellestablished that it isconsidered the mostcommon and successfultransplant operation inmedicine today.

Corneal transplantsare done for a variety ofconditions that affectthe cornea. The corneais the clear windowlikecovering for the eye,

which focuses light on the reti-na and protects the internal eyefrom injury. Corneas can bedamaged by injury; infectionincluding herpes; inherentcorneal disease such as kerato-conus, a thinning of the cornealtissue, or corneal dystrophysuch as Fuchs’ Dystrophy, aprogressive dysfunction of thecorneal endothelial cells; or pre-vious eye surgery.

A transplant becomes neces-sary when disease or injuryscars the cornea enough tobecome opaque and incapableof delivering a sharp image tothe retina. Replacing a damagedcornea can restore clarity tovision, and quality to life.

As with other transplant sur-geries, in corneal transplan-tation diseased tissue (hostcornea) is replaced by healthytissue (donor cornea). Thedonor cornea comes from

someone who has died anddonated his or her eyes for the benefit of others.

Unlike other transplantedtissue, corneal tissue does notrequire extensive type matching.Cause of death, length of timebetween death and transplant,and the presence of donor eyedisease are the determining fac-tors. Also, because the corneahas few blood vessels andbecause of the eye’s naturalimmune suppression (see Ask aSchepens Scientist on page 6),corneal transplants are less fre-quently rejected by the bodythan other transplanted tissue.

The surgery itself is painlessand straightforward, typicallytaking less than one hour in an uncomplicated case. Mostcorneal transplants are doneunder local anesthesia on anoutpatient basis. During thesurgery, a surgeon carefullyremoves a part of the diseasedcornea and replaces it with thedonor tissue, cut precisely to fit,and then sews it into place withtiny sutures.

During recovery patients areencouraged to refrain from lift-ing heavy objects, and bendingor straining. Water should notbe allowed in the operated eyeuntil the surface cells havehealed (usually one to twoweeks). An eye shield is worn at night for at least one monthafter surgery. Medicated eyedrops (including antibiotic andsteroid eye drops) are used, fre-quently at first, to help preventinfection and calm inflammation.

clinically speaking...

Kathryn Colby, M.D.,Ph.D.

(continued on page 15)

11

The Third Annual Boston Eye Ball, “A Night for Sight,” was held at theFairmont Copley Plaza Hotel on Novem-ber 15, 2002. The guests enjoyed a wonderfulevening of dinner, dancing, and a silentauction.

Mark your calendar now to attend theFourth Annual Boston Eye Ball—Friday,November 14, 2003.

The Eye Ball”A Night for Sight”

November 15, 2002

Remarks from Board Chairman JayWalton

Music by the Bo Winiker Band

Musical performance by pianist DavidCrohan

Shown left to right: Jerre Gowdy, Honorary Co-Chair; J. Wayne Streilein, M.D., President; Rosalie Cohen, Co-Chair; and Curt Gowdy, HonoraryCo-Chair

12

Friends f

The New York area “Friends of The Schepens” and theJewish Guild for the Blind collaborated to host a small tourof an exhibit from the Ralph Esmerian collection at theAmerican Folk Art Museum in New York preceding theMay 22 Eye and Vision Research Seminar held at theHarvard Club. SERI Trustee and Chairman of the NewYork City “Friends of The Schepens,” Ted Voss, hosted areception following the tour.

Tour of the American Folk Art Museum andReception Preceded New York Symposium

Dr. Mara Lorenzi from the Institute discussed“Diabetes and Diabetic Retinopathy.”

Left to right: David Korb, Holly Grieg, Ted Voss, and Dr. J. WayneStreilein at the reception following the tour.

Left to right: David Denniston, Susan Rich,Allan Patt, and Norbert Ratliff.

13

The Schepens

The Palm Beach Area “Friends ofThe Schepens” hosted a Vision for theFuture luncheon at the Mar-A-LagoClub in Palm Beach on Thursday,April 4.

At the luncheon, neuroscientistMichael Young, Ph.D., presented anddiscussed the results of his state-of-the-art research being conducted inthe Minda de Gunzburg ResearchCenter for Retinal Transplantation atThe Schepens Eye Research Institute.

Chairwoman of the event, Herméde Wyman Miro, assisted by KathrynVecellio, Judy Grubman, and Cheryl Gowdy, helped the Institute in creating an educational and informative event.

Left to right: Judy Grubman, Member of “Friends of The Schepens”;Kathryn Vecellio, Trustee and Florida State Chairperson; Cheryl Gowdy,Chairwoman, “Friends of The Schepens,” Palm Beach; and Hermé deWyman Miro, Honorary Founding Chairwoman, “Friends of TheSchepens.”

Vision for the Future Luncheon

With the support of the New York area “Friends ofThe Schepens,” the Institute honored Henry Grunwaldwith the Man of Vision Award at the “Vision for theFuture Luncheon” on October 15 at the Mutual ofAmerica Ballroom in New York City. Mr. Grunwald is the former editor-in-chief of Time, Inc., former USambassador to his native Austria, and author of Twilight,a personal account of his struggle with macular degen-eration. The award was presented by Sharon King Hoge,a member of the New York “Friends of The Schepens”committee.

In conjunction to the award presentation, ScientistMichael Young, Ph.D., a neurobiologist at The SchepensEye Research Institute, presented promising researchinvolving retinal transplantation and stem cell researchthat may one day lead to regeneration of retinas dam-aged by disorders such as macular degeneration.

Henry Grunwald receiving his Man of VisionAward from Sharon King Hoge of the New YorkChapter of “Friends of The Schepens.”

Man of Vision Award

14

do-fovea develop in the area of the retina where a person isbest able to deploy their visualattention.

This information will help us better understand why pseu-do-fovea develop where they do and may lead to improve-ments in vision rehabilitation.Ultimately, it will help us devel-op the skills in patients thatthey need to improve theirreading, according to Fine.

The work that Fine lovesmay help Ina Ward return to an activity she loves andmisses.

Improving facial recognition“Most facial features are

of low contrast anyway, justshadows of the structure of theface,” says Eli Peli, O.D., a sen-ior scientist at The SchepensEye Research Institute. “Imaginehow blurred or broken visioncan contribute to the difficultyof recognizing a face,” he says.

Peli has been studying face-recognition skills for a numberof years. He shows patientsphotos of celebrities that havebeen enhanced in differentways and asks them to ranktheir certainty that a particularindividual is a celebrity on ascale of one to five. He hasfound the greatest improve-ment in recognition (when a picture is enhanced) forpatients who were originallythe most impaired.

His studieshave also ledhim to testdevices thatcan restorerecognitionskills. “If youmove closer to or magnifya face, itbecomes morerecognizable even when thecentral vision is blurred ornearly missing,” he says.According to Peli, “while thecontrast doesn’t change, theretina has a better sensitivity to larger rather than to smallerthings.”

According to Peli, a devicelike a bioptic telescope mount-ed on a pair of glasses canmake it possible for Ina Wardto recognize her friends andfamily at a distance with aquick telescopic glance. Peli is also developing and testingenhanced-contrast televisionsand a portable video camera

attached to a pair of videoglasses which enhance outsideimages as a person with AMDwalks around.

These are just a few of theresearchers at The SchepensEye Research Institute whoare investigating AMD.Others will be featured infuture issues of Sightings.

“Because AMD can be devastating to a person’s life

and lifestyle, earlydetection, future

prevention if possible,and access to

rehabilitation areessential.”

Eli Peli, O.D., SeniorScientist

Stolen Sight (continued from page 5)

“Scientific American Frontiers.”“Knowing that I am supportingresearch that may spare thosein the future from the pain thatBen experienced gives me sucha wonderful feeling.” Madelonfeels so strongly about support-ing the Institute’s future researchthat she is providing in her willto donate any lifetime paymentsshe receives from her Charita-ble Gift Annuity back to theInstitute.

Madelon’s message to thosewhose lives have been affectedby blinding diseases is twofold.“Seek counseling to deal withthe emotional and psycho-logical effects of blindness, and support the work of The Schepens Eye ResearchInstitute.”

To learn more about how aCharitable Gift Annuity canhelp you further your philan-thropic and financial objectives,please contact George Constant,Director of Planned Giving, at(617) 912-2572 or (877) 724-3736 (toll free), or constant@vision.eri.harvard.edu.

Profiles in Philanthropy(continued from page 7)

15

Clear, unimpeded vision canbe a matter of life and deathfor a pilot, a soldier, or a navalofficer, and protecting thatvision is the goal of militaryeye specialists. Eighteen of themilitary’s most skilled ophthal-mologists and optometristsspent two full days at TheSchepens Eye Research Institutethis September to share theirexperiences, problems, andconcerns with Schepens scien-tists and discuss and developpossible research solutions.

“We were thrilled to meetthis illustrious group of physi-cians who gave us a firsthandaccount of the special eye carechallenges faced by our mili-tary,” says J. Wayne Streilein,M.D., president of The SchepensEye Research Institute. Accord-ing to Dr. Streilein, the ultimategoal of the symposium was forThe Schepens Eye ResearchInstitute to propose researchprojects that in the short termaddress urgent needs of thosein combat and that in the longterm enhance the lives of all

people dealing with visualimpairment.

Each year, scientists andmedical researchers around thecountry are granted fundingfrom the U.S. Defense Depart-ment’s TATRC, which standsfor Telemedicine AdvancedTechnology Research Center.The Schepens Eye ResearchInstitute has been a consistentrecipient of funds from thatorganization. This year is thefirst time that TATRC hascome to the Institute to talkabout the full range of theirconcerns about eye care in the military.

One full day of the sym-posium was devoted to the mil-itary’s recent use of refractivesurgery (laser corrective sur-gery) to eliminate some of thedifficulties created by glassesand contact lenses in combatsituations. Although the use ofthis surgery has dramatic posi-tive effects, it also can haveserious drawbacks such as slowwound healing and haze thatcan suddenly appear in treated

eyes which can leave a militaryperson unable to function in aremote location. Night visionmay also be an issue, some-times helped by refractive sur-gery, sometimes made worse.And at this point, the militarydoes not have a good methodfor assessing function in lowlight after surgery.

Among the topics discussedon the second day of the sym-posium were battlefield injuriesin Desert Storm and Kosovo,corneal/globe wound stabiliza-tion, retinal laser injuries, andterrorism and bio-terrorism and the eye.

At the conclusion of thesymposium, Dr. Streilein wasable to present the militarywith a number of ways that TheSchepens Eye Research Institutemight help, including devicesfor simulating flight conditionsto test low light vision, thecreation of a special cornealbandage to protect the eye afterinjury, and wound healing tech-niques already under develop-ment at the Institute.

Ocular Challenges for the 21st-Century Military

Over the course of the nextyear, the surgeon may need toadjust the shape of the newcornea by manipulating thesutures. It typically takes six to nine months after cornealtransplantation for the visionto stabilize. The degree towhich vision improves and howlong that improvement lastswill depend on the state of theoriginal eye disease or injury.

Of course, as with all sur-gery, there can be compli-cations, and with cornealtransplants they can range from infection and inflamma-tion to glaucoma or retinaldetachment. However, theoverall complication rates are very low.

So my advice to you is tohave a heart-to-heart discussionwith your physician to deter-

mine what your particularneeds and risks are. If cornealtransplantation is what youchoose, your chances of im-proving your vision are veryhigh, and good results can last for many years.

Clinically Speaking (continued from page 10)

16

So what does this mean forautoimmune diseases? Auto-immune diseases occur whenthe body mistakenly sees itstissues as a foreign intruderand attacks itself. This attackon itself can cause such dis-eases as uveitis in the eye,diabetes in the pancreas andmultiple sclerosis in the spinalcord and brain. The ringleadersin this process are auto-reactiveT cells.

We theorized that we coulduse alpha-MSH to make regu-latory T cells outside the bodyand then when they were rein-jected into the body, theywould turn off the T cells caus-ing autoimmune disease. Forexample, uveitis, a blinding

inflammation of the retina,might be cured by this tech-nique. We also hypothesizedthat we could inject alpha-MSH into a uveitic eye andsuppress the inflammation. Inboth cases, we accomplishedour goal and suppressed auto-immune uveitis in experimentalanimals.

Now a pharmaceutical(biotech) company is workingwith our discovery to develop aproduct that we believe couldhelp millions of people. If suc-cessful it could not only affectautoimmune diseases, but itcould also prevent rejection of other types of organ trans-plants.

The next phase of ourresearch will focus on usinggene therapy to promote theexpression of alpha-MSHinside the body to prompt theactivation of regulatory T cellswithout the need to treat T cellsoutside the body.

Beyond that, we are also try-ing to understand, why, in lightof so much local immunosup-pression, the eye is so highlyresistant to bacterial infections,even when bacteria have beenintroduced into the eye. Theanswer may also lie with alpha-MSH and the other suppressivefactors we have found in theeye.

Ask a Schepens Scientist (continued from page 6)

THE SCHEPENSEYE RESEARCH INSTITUTE20 Staniford Street, Boston, MA 02114

V E R I TAS

An affiliate of Harvard Medical School

Address Service Requested

NON-PROFIT ORG.U.S. POSTAGE

PAIDPERMIT NO. 75

RANDOLPH, MA