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Thread: OEG Treatment of ALS

  1. #41
    Junior Member
    Join Date
    Jan 2005
    Ouro Fino, MG, Brasil
    Hi Dr. Wise!

    We are so surprise with this comunity!
    You are sky angels.

    We are from Brasil. My uncle has ALS in early stage.

    I want to kwow what do you think about Biomark Cia. They send by $18.000 (euros) a injection of stem cells for ALS tratament.

    It's results like chineses Dr. Huang's brain surgery in PALS. The testemunal in site are unbeliveble.


    I have to do something. I can't stay wacthing my uncle and my family in this condiction.

    Or Beijing or Biomark.

    What do you thing about?

    Help us.


  2. #42

    I don't think that the treatment being offered by this Biomark International is based on sound scientific information. Let me first review available evidence for umbilical cord blood effects on spinal cord injury and then on amyotrophic lateral sclerosis.

    Spinal cord injury. Although a few studies have reported that CD34+ umbilical cord blood cells transplanted directly into spinal cord may improve recovery in rats after injury (Zhao, et al., 2004; Li, et al., 2004) and one study suggested that intravneous infusion human umbilical cord blood into rats can improve recovery after spinal cord injury (Saporta, et al., 2003), all these studies gave the cells shortly after injury. CD34+ is also a marker of hematopoietic cells (i.e. cells that make blood cells) as opposed to cells that make neurons or glia. To my knowledge, nobody has shown that intraspinally transplanted umbilical cord blood cells replace neurons or stimulate regeneration in chronically injured animal spinal cord. There was one report that Koreans have transplanted well-matched human umbilical cord blood "stem cells" into the spinal cord of a patient at 20 years after injury and apparently improved her walking but, as I have explained before, this is only one case and it is not clear how much she improved and whether the transplant was responsible.

    Amyotrophic Lateral Sclerosis. Garbuzova-Davis, et al. (2003) reported that transfusion of G93A SOD1 mice (a mouse that has a gene known to cause ALS) with human umbilical cord blood delayed disease progression by 2-3 weeks and increased survival of the mice. They claim that the cells migrated into the brain and spinal cord of the mice, and expressed neural markers. I have read this study and am not convinced that they have shown that the cells have replaced motoneurons. However, the cells may have protected or slowed down degeneration of the motoneurons. Ende, et al. of New Jersey Medical School in Newark ( had likewise reported that human umbilical cord blood slightly improved survival of SOD1 mice from 127 days to 148 days. Please note, however, that both these experiments gave HUGE doses of human umbilical cord blood to the mice and immunosuppressed them. For example, Ende, et al. irradiated the mice with 800 cGy and then infused 35 million mononuclear human umbilical cord blood. For comparison, I think that the telemark treatment is about 5 million CD34+ cells to a human. A mouse weighs 20-30 grams compared to a 50-60 kg human.

    Dr. Mitchell Ghen in Atlanta and Dr. Daniel Cosgrove treated 9 ALS patients in Atlanta (source: ALS TDF) with umbilical cord and placental blood cell infusions. Even anecdotal results apparently have been quite mixed. Several patients thought that the treatment had a very positive effect which others thought that it had no effect or may have even made them worse. ALSTDF and ALSA are trying to facilitate a clinical trial of umbilical cord blood treatment to determine whether the treatment is safe and effective.

    An Atlantic Journal and Constitution story in March 29, 2003 reported that the FDA investigated Dr. Ghen and contacted the Florida blood bank that was supplying him. Dr. Ghen stopped providing the transfusion. Apparently, Dr. Cosgrove also stopped providing the treatment after learning of the FDA investigation. Apparently, the patients paid $25,000 but they received up to 20 units of cord blood (a lot). Please note that a number of unscrupulous physicians have made unwarranted claims for umbilical cord blood therapies of Parkinson's disease and other conditions (see: Cord Blood Research)


    References cited

    1. Zhao ZM, Li HJ, Liu HY, Lu SH, Yang RC, Zhang QJ and Han ZC (2004). Intraspinal transplantation of CD34+ human umbilical cord blood cells after spinal cord hemisection injury improves functional recovery in adult rats. Cell Transplant. 13: 113-22. National Research Center for Stem Cell Engineering & Technology, State Key Laboratory of Experimental Hematology, Institute of Hematology, Chinese Academy of Medical Sciences, Peking Union Medical College, Tianjin, People's Republic of China. The present study was designed to compare the functional outcome of the intraspinal transplantation of CD34+ human umbilical cord blood (CB) cells with that of human bone marrow stromal (BMS) cells in adult rats with spinal cord injury. Sixty adult Wistar rats were subjected to left spinal cord hemisection, and then divided into three groups randomly. The control group received an injection of PBS without cells, while the two other groups of rats received a transplantation of 5 x 10(5) CD34+ CB or BMS cells, respectively. Functional outcome was measured using the modified Tarlov score at days 1, 7, 14, 21, and 28 after transplantation. A statistically significant improvement in functional outcome and survival rate in the experimental groups of rats was observed compared with the control group. Rats that received CD34+ CB cells achieved a better improvement in functional score than those that received BMS cells at days 7 and 14 after transplantation. Histological evaluation revealed that bromodeoxyuridine (BrdU)-labeled CD34+ CB and BMS cells survived and migrated into the injured area. Some of these cells expressed glial fibriliary acidic protein (GFAP) or neuronal nuclear antigen (NeuN). Our data demonstrate for the first time that intraspinal transplantation of human CD34+ CB cells provides benefit in function recovery after spinal cord hemisection in rats and suggest that CD34+ CB cells may be an excellent choice of cells as routine starting material of allogenic and autologous transplantations for the treatment of spinal cord injury.

    2. Li HJ, Liu HY, Zhao ZM, Lu SH, Yang RC, Zhu HF, Cai YL, Zhang QJ and Han ZC (2004). [Transplantation of human umbilical cord stem cells improves neurological function recovery after spinal cord injury in rats]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 26: 38-42. State Key Laboratory of Experimental Hematology, Institute of Hematology, CAMS and PUMC, Tianjin 300020, China. OBJECTIVE: To study whether intraspinally transplanted human cord blood CD34+ cells can survive, differentiate, and improve neurological functional recovery after spinal cord injury in rats. METHODS: Rats were randomly divided into two groups. One group of rats was subjected to spinal cord left-hemisection and transplanted with human cord blood CD34+ cells labeled by bromodeoxyuridine (BrdU); The other group was carried by left-hemisection with injection of PBS (control group). The neurological function was determined before and 24 h, 1, 2, 3 and 4 weeks after spinal cord injury and cell transplantation using the modified Tarlov score. The distribution and differentiation of transplanted human cord blood cells in vivo in rat spinal cord were evaluated by histological and immnuhistochemical analysis. RESULTS: Functional recovery determined by modified Tarlov score was significantly improved in the group receiving human cord blood CD34+ cells compared with the control group (P < 0.05). Moreover, human cord blood CD34+ cells were found to survive in rat spinal cord microenvironment, with the expression of the neural nuclear specific protein [NeuN) in 2% BrdU-reactive human cells and of the astrocytic specific protein glial fibrillary acidic protein [GFAP) in 7% BrdU-reactive human cells. CONCLUSIONS: Intraspinally administered human cord blood CD34+ cells can survive, differentiate, and improve functional recovery after spinal cord injury in rats. Transplantation of human cord blood cells may provide a novel strategy for the treatment of neural injury.

    3. Garbuzova-Davis S, Willing AE, Zigova T, Saporta S, Justen EB, Lane JC, Hudson JE, Chen N, Davis CD and Sanberg PR (2003). Intravenous administration of human umbilical cord blood cells in a mouse model of amyotrophic lateral sclerosis: distribution, migration, and differentiation. J Hematother Stem Cell Res. 12: 255-70. Center of Excellence for Aging and Brain Repair and Department of Neurosurgery, University of South Florida, College of Medicine, Tampa, FL 33612, USA. Amyotrophic lateral sclerosis (ALS), a multifactorial disease characterized by diffuse motor neuron degeneration, has proven to be a difficult target for stem cell therapy. The primary aim of this study was to determine the long-term effects of intravenous mononuclear human umbilical cord blood cells on disease progression in a well-defined mouse model of ALS. In addition, we rigorously examined the distribution of transplanted cells inside and outside the central nervous system (CNS), migration of transplanted cells to degenerating areas in the brain and spinal cord, and their immunophenotype. Human umbilical cord blood (hUCB) cells (10(6)) were delivered intravenously into presymptomatic G93A mice. The major findings in our study were that cord blood transfusion into the systemic circulation of G93A mice delayed disease progression at least 2-3 weeks and increased lifespan of diseased mice. In addition, transplanted cells survived 10-12 weeks after infusion while they entered regions of motor neuron degeneration in the brain and spinal cord. There, the cells migrated into the parenchyma of the brain and spinal cord and expressed neural markers [Nestin, III Beta-Tubulin (TuJ1), and glial fibrillary acidic protein (GFAP)]. Infused cord blood cells were also widely distributed in peripheral organs, mainly the spleen. Transplanted cells also were recovered in the peripheral circulation, possibly providing an additional cell supply. Our results indicate that cord blood may have therapeutic potential in this noninvasive cell-based treatment of ALS by providing cell replacement and protection of motor neurons. Replacement of damaged neurons by progeny of cord blood stem cells is probably not the only mechanism by which hUCB exert their effect, since low numbers of cells expressed neural antigens. Most likely, cord blood efficacy is partially due to neuroprotection by modulation of the autoimmune process.

    4. Ende N, Weinstein F, Chen R and Ende M (2000). Human umbilical cord blood effect on sod mice (amyotrophic lateral sclerosis). Life Sci. 67: 53-9. Department of Pathology and Laboratory Medicine, UMDNJ-New Jersey Medical School Newark, USA. In previous studies we observed that human umbilical cord blood (HUCB) could have a protective effect on the onset of disease and time of death in MRL Lpr/Lpr mice which have an autoimmune disease that may be considered similar to human lupus. We believed a temporary xenograph may have occurred in these animals with the disease process delayed and the life span markedly increased. When HUCB is stored at 4 degrees C in gas permeable bags, there is a decrease of the cell reaction in mixed lymphocyte cultures. The blood, however, maintains a significant number of cells capable of producing replatable colonies. This study attempted to determine the effect of HUCB on SOD1 mice (transgenic B6SJL-TgN(SOD1-G93A)1GUR), which have a mutation of the human transgene, (CuZn superoxide dismutase gene SOD1) that has been associated with amyotrophic lateral sclerosis. We previously developed evidence that the survival of lethally irradiated mice was related to the number of human mononuclear cells administered. In the present study, we decided to investigate the effect of a relatively large dose of human mononuclear cord blood cells on SOD1 mice subjected to a sublethal dose of irradiation preceded by antikiller sera (rabbit anti-asialo). The SOD1 mice show evidence of paralysis at 4 to 5 months. The average expected lifetime of these mice is reported to be 130 days (Jackson Laboratory). In this experiment, there were 23 mice. Two mice died before the onset of paralysis. The remainder were divided into three groups: group I: control group of 4 untreated mice; group II: an experimental group of 6 mice treated with antikiller sera, 800 cGy irradiation plus 5 x 10(6) congenic bone marrow mononuclear cells; group III: another experimental group of 11 mice treated with antikiller sera, 800 cGy irradiation plus 34.2-35.6 x 10(6) HUCB mononuclear cells, previously stored for 17-20 days at 4 degrees C in gas permeable bags. The results were as follows: the average age at death was: (I) 127 days for the untreated control group, (II) 138 days for the group that received 800 cGy of irradiation and congenic bone marrow (BM) and (III) 148 days for the group that received irradiation and HUCB. (P < 0.001 HUCB vs control, p < 0.01 HUCB vs BM). The longest surviving mouse in each group was 131, 153, and 182 days old respectively. In summary, large doses of HUCB mononuclear cells produced considerable delay in the onset of symptoms and death of SOD1 mice. These preliminary results may not only indicate that amyotrophic lateral sclerosis is an autoimmune disease, but may also indicate a possible treatment for a devastating disease and possibly others.

    [This message was edited by Wise Young on 01-21-05 at 01:35 AM.]

  3. #43
    Senior Member
    Join Date
    Apr 2002
    katonah , ny, usa
    Dr. Young- If ALS kills motor nerves in the brain and spinal cord, couldn't this procedure help someone like me with a SCI to my anterior Lumbosacral grey horns? My SCI has to do with infarction of grey matter, couldn't this apply to SCI as well as ALS?

    sherman brayton

  4. #44

    Dr young just wondering what your thoughts were regarding Brayton's question as it applies to grey matter injuries.


  5. #45
    Sherman, as far as I can tell, no study has shown that OEG cells replace neurons, particularly motoneurons. I think that the hope is that the cells will slow down the motoneuronal degeneration. Wise.

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