THE
Myelin PRoject
Winter Newsletter 2008
2008
THE YEAR IN REVIEW
As we look back over 2008,
for the progress reports on these
we see a year filled with excitement
research projects.
about the direction of The Myelin
The Myelin Project is being
Project and sadness because we
featured in the Public Broadcasting
lost our Lorenzo this year. As
System Giving Back Series: Heroes
most of you know Lorenzo Odone
in Health. This mini-documentary
passed away on May 30, 2008,
will air on PBS affiliates across
one day after his 30th birthday.
the country. A public service
announcement was produced
We want to take this opportunity to
along with the mini-documentary.
thank everyone who sent messages
Further information regarding both
of condolence to Lorenzo’s father,
the documentary and the public
Augusto Odone. He has asked
service announcement is available
that we thank each of you for your
through our office, at 800-869kind words of sympathy during this
3546.
difficult and sad time.
We would like to send
As we enter 2009 we celebrate
a special thank you to Jane
the 20th anniversary of The
Rosenthal, John and Pat Bloomquist
Myelin Project. It is a bittersweet
and the fabulous staff at the
anniversary. We were hoping
Owenego Inn for allowing us to
that in 20 years we would have
film at their picturesque Inn located
made better progress to restore
In Loving Memory
in Branford, Connecticut.
myelin. Even though that has not
Lorenzo
Odone
We have had tremendous
occurred, the scientific community
May 29, 1978 to May 30, 2008
response from schools worldwide
is in agreement that major progress
to our educational program “Using Lorenzo’s Oil as
has been made. The Myelin Project has been and
a Teaching Tool”. The film “Lorenzo’s Oil” raises
will continue to be a driving force in remyelination
important scientific and ethical questions. The study
research.
guide is intended to assist teachers in facilitating
During the last year our web site has had over
classroom discussions of these questions. If your
230,000 hits from 176 countries. More than 12%
school is interested in utilizing the program please
of these visitors were from Latin America, indicating
contact our office, at 800-869-3546
a definite need to reach out to these people in their
The Lorenzo’s Oil Clinical Trial currently underway
native languages. We are proud to announce that
at the Kennedy Krieger Institute in Baltimore, MD is
the home page of our web site has gone trilingual!
accepting boys who carry the ALD gene, and who
www.myelin.org is now available in both Spanish
meet the criteria for participation in the study. For more
and Portuguese. We are very grateful to Moises
information please contact Kim Hollandsworth at the
Herrezuelo Lopez from Spain and Andre Viana from
Kennedy Krieger Institute in Baltimore, Maryland (443)
Brazil, who provided the translations services to the
923-2750 or you may email her at hollandsworth@
Myelin Project free of charge.
kennedykrieger.org.
The Myelin Project funded over $185,000 in
research grants during the past year. Please see the
section “News from the Laboratory” in this newsletter
Continued on Page 2
www.myelin.org
Acknolwedgments
We are grateful to all of you who contributed to The Myelin Project this year and are honored that you continue
to support us and our cause. We want to take this opportunity to publicly acknowledge your generosity.
Platinum - $5000 and up
Race Productions – Ron Meneo
Lemonade Gang – Branford, CT
Porter E. and Helenmae Thompson Foundation
Barbara Daniell
Daniell Family Foundation
J. Michael Johnson
Jack and Jean Kelley
Chris Kaag
Larry and Patti Chapman
Stennis Foundation
Gold - $2000 - $4999
Karen Fleming/Northwood School, Lake Placid
Debra Dill-Bergmann
Anthem Blue Cross/Blue Shield – New Haven, CT
Robert and Laura Massey
Kevin O’Neill
Andrea Sargeant
J. F. Sattler
Paul Sturgess
Aaron Swan
Richard Smith
Town Fair Tire Center
Kathryn Tutino
V.F. McNeil & Company
Wells Fargo Community Support Campaign
First Giving.com
Just Give.com
Silver - $1000 – $1999
John Wynne
John Buckley
Kathy Glover
Spartanburg County Schools, SC
Paul and Corie Barraco
Sheree Bodary
Brenner, Saltzman and Wallman
Brookwood Financial Partners
George Cahill
Edward Crowley
John Davis
James R. Delmore
Steven Decker
Chip and Helen Fedalan
Gillis & Gillis, P.C.
Robert and Theresa Goodman
Robert Hacker
Michael T. Heffernan
Donald Herzog
Robin and Joanna Michel Charitable Gift Fund
Yale-New Haven Hospital
Bronze - $500 - $999
Harold Rounds
Timothy Sloan
Michael and Cheryl Marino
Michael Martino
Douglas Chubb
George Brencher, IV, PC
Gino and Sonja Buffa
Kirsten Stauffer
Mark Augusti
Sharon Lee Baird
Dr. John Beiner
Branford Rotary Club
George Brencher
Melanie Cameron
Douglas Chubb
Glen Clark
Steven Decker
Karen Fleming
Craig and Shari Friedman
Jay and Jill Gold
Sid and Sharon Granetz
Jack and Barbara Greenberg
JJ and DE Holler
Paul Kelley, DDS
William and Barbara Lyons
MFG Partners, Inc.
McCallum, Mr. and Mrs. John McCallum
Thomas Moran
Harry Tortello
Gary Vogel
Rode and Elaine Wanta
Mark and Virginia Ziegenfuss
Year in Review continued from Page 1 We would like to take this opportunity to recognize
and thank Myelin Project board members Jean Kelley
(Hammerfest Triathlon, Brian’s Beachside Boogie)
and Chris Kaag (Got the Nerve Triathlon) for their
continuing fundraising in behalf of The Myelin Project.
This year, their events, involving more than 1000 race
participants and 300 volunteers, raised over $75,000.
We also want to convey our sincere gratitude to
Ron Meneo of Race Productions, New Haven, CT.
In addition to producing Hammerfest Triathlon and
Brian’s Beachside Boogie, Race Productions donated
$9,000 to The Myelin Project. Last, but certainly not
least, our sincere gratitude to The Lemonade Gang of
Page 2
Branford, CT. This group of young people, led by Ryan
Bloomquist and Greg Noble, raised $8,000 for The
Myelin Project this year.
These donations have been designated to help
fund the development of a newborn screening test for
ALD. Please see the “News from the Laboratory” for
an update on this important project.
If you are interested in hosting a triathlon or a
fundraising walk in your community please contact us
(800-869-3546). We will gladly assist you by sharing
our expertise, providing race director’s handbooks
and generally guiding you through the process of
conducting a successful event.
News
From The
Laboratory
Dr. Ian Duncan’s group from the University of Wisconsin summarized three new (and as yet
unpublished) projects. Two of them involved research on a mutant mouse (op) that is not able to develop
certain cell types that are important in bone remodeling and in the immune system.
The first project studied the numbers of microglial cells, which are part of the immune system in the central nervous system.
The microglia are important in diseases of brain inflammation, such as multiple sclerosis. Dr. Duncan’s lab found that there are
fewer microglial cells in the white matter of op mice as compared to control mice. However, the numbers of microglia in the
grey matter were not different between the two groups. While microglia in both mutant and control mice responded to a wound
in the cerebral cortex (part of the brain grey matter), the change in the op mice was less than the control. These findings make
the op mouse a useful model in which to explore the role of microglia in inflammatory diseases.
The second project on the op mouse studied the optic nerve. Because op mice have abnormal bone remodeling, the
surrounding bone compresses their optic nerve. At the compression site, there are few oligodendrocytes, the cells that make
brain myelin. So, there is little or no myelination at this site. Nerve conduction through the area of non-myelination is severely
affected. The group plans to study whether the oligodendrocytes die because compression reduces their blood supply.
Finally, Dr. Duncan reported on a new model of chronic demyelination and remyelination in the cat, induced by feeding
the animals an experimental diet. Only the myelin sheath appears to be affected, with axons remaining intact. When the
cats are returned to a normal diet, they recover neurologically with evidence of remyelination throughout the entire CNS. This
model proves unequivocally, and for the first time, that remyelination restores function in a large animal model and confirms that
remyelination is a major therapeutic target in demyelinating disease.
Professor Neil J. Scolding, FRCP PhD, University of Bristol Institute of Clinical Neurosciences, U.K.,
provided a report of his studies of bone-marrow derived cells for the treatment of multiple sclerosis.
About 30 years ago, investigators began to think that cell therapies might be useful to treat loss of myelin caused by multiple
sclerosis (MS). The disease has proved more complex, and tissue repair in the brain and spinal cord more challenging than we
first thought. Many factors contribute to myelin and nervous tissue damage in MS. Cells capable of myelin repair are present
in damaged areas but nonetheless do not seem to repair myelin. This might mean that simply adding more myelin-making cells
to lesions won’t be enough to help in this disease. Professor Scolding is studying bone marrow derived stem cells. These have
a very limited capacity for turning into myelin forming cells. But they seem to stimulate repair processes that are key to tissue
regeneration in MS. A small safety study of these cells in six patients with chronic MS is nearing completion. The final report
will be made when the data analysis is finished. Dr. Scolding has said, “We are grateful indeed to the Myelin Project for our
funding, without which this trial would have proved very difficult to complete.”
Dr. Gianvito Martino of the San Raffaele Institute in Milan, Italy reported on the therapeutic plasticity
of neural stem cells.
Recent evidence challenges the conventional view that neural stem/precursor cells (NPCs) protect and repair the central
nervous system (CNS) simply by replacing damaged cells. Rather, NPCs may also promote CNS repair by a “bystander”
effect. In other words, NPCs may release a mixture of neuroprotective molecules at the site of tissue damage. These protective
substances are released in a coordinated manner, in response to the specific needs of the damaged tissue. Even in undamaged
tissue, NPCs produce these molecules, which help to maintain nerve tissue throughout life. These protective agents may be
common to many kinds of somatic stem cells (e.g. mesenchymal stem cells). These kinds of stem cells don’t normally differentiate
into neural cells, yet they may efficiently promote CNS repair. Thus, the repair capacity of stem cells may well include their
ability to adapt their fate and function(s) to specific needs in response to different pathological conditions (therapeutic plasticity).
The discovery that transplanted NPCs may protect the brain through bystander strategies is of pivotal importance for the future of
stem cell based therapeutics.
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Professor Robin Franklin, Cambridge Center for Brain Repair, University of Cambridge, U.K., related
how studies in his laboratory demonstrate an unexpected connection to other aspects science.
Over the last year Dr. Franklin’s lab has been continuing its work on how the brains own stem cells are able to replace
lost myelin-forming cells (oligodendrocytes). Doing so is expected to help identify therapeutic targets that will help to enhance
remyelination in patients. In collaboration with other laboratories several new pathways have been identified that either
encourage or prevent stem cells becoming new oligodendrocytes. At this year’s meeting Professor Franklin explained how
some of these pathways are also involved in the formation of cancers. Of course, cancer scientists have for some time been
developing drugs to influence these pathways. Thus, some of the developments that are being made in cancer treatment may,
unexpectedly, have additional roles in encouraging myelin regeneration in myelin diseases. There is still some distance to go in
realizing the potential of such approaches but current signs indicate that this is a promising line of investigation.
Dr. Anne Baron-Evercooren, Centre Hospitalier Universitaire, Pitié-Salpêtrière, Paris, presented her
investigation of how Schwann cells might be altered so that they might be better candidates for myelin
transplantation. By forcing the cells to express an enzyme, sialyltransferase, their ability to migrate was
greatly improved.
Schwann cells (SC) form myelin in the peripheral nerves and are easy to get. Despite their obvious repair potential in
the central nervous system (CNS), several studies indicated that SC aren’t effective in repairing CNS myelin. Other cell types
(olfactory ensheathing cells, neural stem cells and oligodendrocytes) can repair CNS myelin, but are not very easy to get. Dr.
Baron-Van Evercooren’s laboratory has explored some of the differences between SC and these other cell types. All of the
myelin forming cells, including the SC, express NCAM, a specific protein, on their surface. However, the NCAM of the CNS
myelin forming cells is “decorated” with a specific carbohydrate, while the NCAM of the SCs is “plain”.
To solve this problem, Dr. Baron-Evercooren and her associates have developed a method of getting SCs to produce
“decorated” NCAM. After characterizing the modified SC cells in culture, they were transplanted to mice that had spinal cord
demyelination. The modified SC were much more efficient at repairing the demyelination than the control SC. These results
underline the potential therapeutic benefit of genetically modifying SC to overcome their poor migratory property and promote
their repair potential in demyelinating disorders of the CNS. Dr. Baron-Evercoorn’s work has been supported by WFL and
INSERM
Violetta Zujovic, Ph.D., Centre Hospitalier Universitaire, Pitié-Salpêtrière, Paris, reported on her work
to identify cell types that might be useful in re-myelination.
During development, the entire nervous system begins as a mass of cells called the neural crest. Boundary cap cells (BC)
are descended from neural crest cells. The BCs migrate to the boundary between the central (brain and spinal cord) and
peripheral (sensory and motor nerves) divisions of the nervous system. BCs are important because they are the ancestors
of Schwann cells (the myelin forming cells of the peripheral nerves). In addition, BCs are also the ancestors of some of the
nocioceptive (pain-sensing) nerve cells of the dorsal root ganglia (part of the spinal cord).
To gain insights in BC’s behaviour in the demyelinated central nervous system, BCs were isolated from developing mouse
brain. When BCs were transplanted to a demyelinated region of a mouse spinal cord, they were able to multiply, thus efficiently
repairing the lesion. When grafted at a distance (one vertebra away) from the lesion, the BCs were not only able to multiply,
but they and their descendents migrated toward the lesion. The migrating cells colonized and repaired the demyelinated lesion.
Interestingly, the BCs were even more efficient at colonizing the demyelinated region than Schwann cells transplanted directly to
the lesion.
Thus, there is evidence that boundary cap cells are able to remyelinate central nervous system axons. This evidence strongly
indicates that boundary cap cells are of interest as a potential method of central nervous system myelin repair.
Page 4
Dr. Alessandra Biffi, M.D., of the San Raffaele Scientific
Institute, Milan, Italy, reported on her group’s advances in
hematopoietic stem cell based gene therapy for the treatment
of metachromatic leukodystrophy.
Metachromatic Leukodystrophy (MLD) is a demyelinating disease
due to inherited deficiency of arylsulfatase A (ARSA). In the absence of
effective therapies, MLD is a disease with an urgent medical need. This is
particularly important, since donor hematopoetic stem cell (HSC) transplant
in MLD has met with mixed results. In a mouse model, ARSA can be
transplanted to the central nervous system. Specifically, the ARSA gene
was transplanted to HSC of MLD mice. Then the modified HSCs were
transplanted back to the MLD mice. After this treatment, the manifestations
of MLD were corrected. Both the feasibility and safety of this therapeutic
strategy were tested in a pre-clinical model. Using HSCs from human MLD
patients, a similar strategy has successfully corrected the ARSA deficiency.
These data have provided the basis for the next step, giving the treated
HSCs back to an MLD patient. This clinical trial of HSC gene therapy for
the treatment of MLD patients is expected to start by the second quarter
of 2009. As in the mouse model, the protocol is based on isolating HSCs
from the MLD patients, transplanting the normal ARSA gene into the HSCs,
then giving the cells back to the patient. This strategy is expected to
avoid the potential complications of graft vs. host disease and to achieve
sustained long term ARSA expression in MLD patients.
Dr. Yoichi Kondo, University of Wisconsin, discussed the
long-term outcome of bone marrow transplantation in a
mouse model of Krabbe’s disease
Bone marrow transplantation (BMT) or umbilical cord blood
transplantation are the only therapies available to date for globoid cell
Leukodystrophy (GLD, Krabbe disease). However, they do not cure the
disease. To discover why, Dr. Kondo investigated twitcher (twi) mice, a
model of GLD. If BMT was performed on these mice 10 days after birth,
the twi mice lived for an average of 168 days. Those animals that did not
receive BMT lived for only about 51 days. When compared to control
twi mice, animals that received BMT had better myelin formation at 45
days of age. However at 200 days, the (twi) mice receiving BMT had
extensive loss of myelin and displayed evidence of progressive neuronal
damage. This study demonstrates that enzyme replacement by simple BMT
is not sufficient for the long-term treatment of GLD.
Dr. Alessandra Biffi also reported on a novel strategy for
gene therapy of globoid cell leukodystrophy.
Globoid leukodystrophy (GLD), also known as Krabbe Disease, is a
genetic disease whose victims are unable to make galactocerebrosidase
(GALC). The GALC enzyme helps to metabolize some of the lipid
components of myelin. A gene therapy strategy for GLD based on
hematopoietic stem cells (HSC) is under development. The gene transfer can
be made by using a virus, called the lentivirus (LV). This has proven to be an
efficient method to transfer the GALC gene to HSCs The treated cells are
able to express GALC at levels that are very high. However, this high level
of GALC expression may also cause functional impairment, or even death,
of the HSCs. It could be that the unnaturally high levels of GALC expressed
by the treated HSCs are damaging to them. However, GALC doesn’t
damage the descendents of HSCs. This suggests a new therapeutic strategy
that is now being tested. The LV vector has been modified, so that when the
GALC gene is transplanted to the HSCs, the GALC gene lies dormant until
the HCS divides and differentiates. That is, the GALC gene is not expressed
until it is safe to do so. This novel strategy avoids GALC damage in HSCs,
while allowing sustained GALC expression in the progeny of the HSCs.
Evaluation of this strategy is in progress.
Page 5
Dr. Celia Kassmann of the Department of Neurogenetics at the Max
Planck Institute for Experimental Medicine discussed her recent studies on
inflammatory neurodegeneration caused by inactivation of peroxisome
function in oligodendrocytes.
X-linked adrenoleukodystrophy (X-ALD) is the most frequent juvenile leukodystrophy. It is
caused by mutations of the adrenoleukodystrophy protein (ALDP), a peroxisomal membrane
protein of unknown function. Attempts to create a mouse model for X-ALD by inactivating the
ALDP gene have failed. Although ALDP deficient mice accumulate very long chain fatty acids
(VLCFA) inflammatory brain demyelination does not occur. Dr. Kassmann investigated how
peroxisomes in oligodendrocytes (the cells that form myelin in the brain) help maintain CNS
myelin. Her laboratory generated a mutant mouse that lacked functional peroxisomes only
in oligodendrocytes. She found that peroxisomes in these cells are essetial for maintaining
white matter (myelin) tracts. The mutant mice developed normally, but within several months
exhibited ataxia, tremor, and premature death. They also showed widespread axonal
degeneration, progressive subcortical demyelination, and a strong brain inflammation. The
exact function of oligodendroglial peroxisomes is still unknown. But, Dr. Kassmann’s studies
suggest that functional peroxisomes are required for axonal support.
Dr. Gerald Raymond, of The Kennedy Krieger Institute, Johns Hopkins University, presented a
summary of current progress in the development of newborn screening in adrenoleukodystrophy
Adrenoleukodystrophy (ALD) is an X-linked disorder that has variable manifestations. In young boys, these may include
adrenal insufficiency and loss of myelin in the brain. In adults, both men and women, there may be a progressive spastic
paraparesis. Boys who inherit the ALD gene require careful monitoring for adrenal and cerebral disease. There are life-saving
interventions for this disorder. Experimental therapy with diet and Lorenzo’s oil may reduce the incidence of childhood cerebral
disease. If these fail, early, appropriate use of hematopoietic stem cell therapy appears to arrest disease progression. However,
these therapies are successful only if begun before clinical symptoms develop.
Virtually all persons with the ALD gene have high levels of very long chain fatty acids (VLCFA) in their plasma. Using this
biochemical abnormality, a method has been developed that can detect elevated VLCFA in very small volumes of blood. This
method is adaptable to regional newborn screening offering early diagnosis and intervention in adrenoleukodystrophy and
other peroxisomal disorders. The sensitivity of the assay was tested in over 500 newborn blood samples, some of which were
from children known to have the ALD gene. The assay was able to identify all of the affected samples. Work is now underway
to test 5000 samples to confirm the sensitivity and specificity. Successful completion of this phase will establish the assay as
a good way to screen all newborn children for the ALD gene. Appropriate monitoring can be initiated immediately. It is
anticipated that this would greatly improve the clinical outcome for these children.
Although Dr. Klaus-Armin Nave, Department of Neurogenetics, Max-Planck-Institute of Experimental
Medicine, was unable to attend the meeting in Ft. Worth, his pre-clinical work on a treatment for
Pelizaeus-Merzbacher disease was presented by his colleague, Dr. Celia Kassmann.
Investigators in Dr. Nave’s lab are using a mutant mouse model to test a new drug therapy for Pelizaeus-Merzbacher disease
(PMD). This severe leukodystrophy is characterized by ataxia, mental retardation, epilepsy and premature death. No therapy is
currently available. Like most humans with PMD, Dr. Nave’s mutant mice over-express the Plp1 gene. So, the mice were used to
test the effect of a new drug (ZK230211) on Plp1 gene expression. Motor function was measured during the 10 week trial. At
the end of the trial, Plp1 gene expression was measured in the brains of the mice. The treated animals expressed 15% less Plp1
than the control mutant mice. Importantly, ZK230211-treated mutants had significantly better motor control. Most relevant, there
were about 30% more myelinated axons in the corticospinal tract of treated mutants, as compared to the controls. This “proof of
principle” trial suggests that it is possible to develop a ‘rational drug therapy’ for PMD patients having Plp1 gene duplications.
We are walking, running, biking and swimming a million miles for myelin research. The
Myelin Project has set a goal to raise $1 million dollars for research to cure demyelinating
diseases. You can help us by donating just $1.00 for each mile you walk, run, bike
or swim to The Myelin Project. This is an excellent opportunity to begin 2009 with
everyone’s favorite resolution to get healthy and loose weight and also help a good cause.
We also want to encourage participants to start their own personal fund raising pages on
www.firstgiving.com and encourage your friends, family and co-workers to sponsor you at
$1.00 per mile. Everyone can afford $1.00 For more details on this fund raising project
please see Million Miles for Myelin on our web site www.myelin.org or contact our office at
1(800) 8myelin (860-3546)
Page 6
Letter from the President
From October 30 to November
bone marrow transplant, and avoids the
2, The Myelin Project held its annual
problem of graft vs. host disease. Dr. Biffi
international meeting in Ft. Worth, Texas.
also stated that a gene therapy strategy
The scientific advances reported are
is under development for treatment of
detailed elsewhere in this newsletter.
GLD. However, there are still a number
Briefly, though, I can tell you that the news
of experiments that remain to be done
is good.
before clinical trials can be contemplated.
For some time, we have known that
After the scientific sessions in Ft.
there are stem cells in the brain, and that
Worth, the boards of the various branches
they are capable of partially repairing
met to discuss and plan the future
the damage done by demyelinating
directions for The Myelin Project. Our
diseases like multiple sclerosis and the
goals, values and vision were discussed
Margaret T. Weis, Ph.D.
leukodystrophies.
and evaluated by representatives from
President
Two laboratories are now on the way to
The United Kingdom, Italy, Germany,
The Myelin Project
a significantly better understanding of how
Canada and the USA. As a group, we
brain stem cells work. Dr. Gianvito Martino
reaffirmed our core purpose:
has discovered that neural stem cells make and release
The Myelin Project exists to end
substances that promote repair of neural tissue. Dr.
the human suffering inflicted by the
Martino calls this the “bystander” effect. It means
demyelinating diseases.
that brain stem cells may act not simply by replacing
Our goal is that myelin will be repaired in humans
damaged cells, but actually help to stimulate brain cells – restoring function – within the next 10 years. We
to repair themselves.
intend to achieve this goal by accelerating the pace
In a different, but related area, Dr. Violetta Zujovic
of applied research that will lead to clinical trials
reports that boundary cap cells, a type of cell that
of myelin repair. Our scientific advisory board is
gives rise to myelin forming cells, are able to find
in the process of drawing up a long-term research
and repair a demyelinated region of a mouse spinal
roadmap leading to our goal. It is the job of the
cord. This may be very significant in the development
various branches to provide the resources necessary to
of myelin transplant procedures. Because the
implement our research plan.
transplanted cells can find the damage by themselves,
We realize that our goal is ambitious, perhaps even
it may not be necessary to transplant cells to every
audacious. But The Myelin Project has a history of
single lesion in order achieve myelin repair.
audacious goals. Twenty years ago, Augusto Odone
Exciting work also continues in developing
dared to believe that ALD could be treated successfully.
strategies to treat metachromatic leukodystrophy (MLD) Not only can it be treated, but universal newborn
and globoid leukodystrophy (GLD, also known as
screening for ALD is in the final stages of testing.
Krabbe Disease). Dr. Alessandra Bifi reported that a
We ask that you join us in our audacious goal
clinical trial for gene therapy of MLD is expected to
of repairing myelin in humans affected by multiple
begin in the second quarter of 2009. The general
sclerosis, the leukodystrophies and other demyelinating
strategy is to take some of the patient’s own bone
diseases. Please help us continue to fund research.
marrow cells, transplant them with a functional
Donations can be made by check, credit card or online
gene, then to replace those cells in the patient. This
at www.myelin.org/en/donations/add.asp.
technique exploits what we already know about
Page 7
The Myelin Project
1400 Wallace Blvd., Suite 258
Amarillo, Texas 79106
MESSAGE FROM AUGUSTO ODONE
As some of you know, Lorenzo passed away, on May 30, one day after his 30th birthday. At
the wish of his late mother, Michaela, he now rests with her in Yonkers, New York. I loved
Lorenzo very much and I can’t think of his passing without crying. I had promised Lorenzo that
I would write a book in his honor when he reached his 30th birthday. He reached this milestone a day before he passed. In keeping with my promise, I am in the process of writing the
book in his memory.
I would like to make a donation to The Myelin Project in the amount of $  Enclosed is my check made payable to The Myelin Project
Name: Address: Phone:
Email:  Charge my gift in the amount of $ ____________ To:
 Visa
 MC
 AmEx
 Disc
Credit Card Number
Exp Date Signature Credit card donations may also be made on our website www.myelin.org
or by calling our office at 800-869-3546
You may also contribute to The Myelin Project at your workplace. Federal employees can donate through the
Combined Federal Campaign (CFC number 11222) You may also donate through the United Way Campaign.
Just enter The Myelin Project name and address on your local United Way donor card.
The Myelin Project is a 501(c) 3 nonprofit organization. Donations are tax deductible to the full extent of the law.
If you wish to
donate to
The Myelin
Project, please
fill out this form
and mail it
back in the selfaddressed envelope included
with this newsletter.
Thank you for
your support.