Dietary iron / neurodegenerative disorders

Discussion in 'Food and nutrition' started by [email protected], Dec 26, 2005.

  1. Abstract View
    <<snip>>
    these data suggest that dietary iron may play a role in the
    vulnerability of neurons to insults associated with PD and other
    neurodegenerative disorders
    <<snip>>

    IRON STATUS INFLUENCES MOTOR BEHAVIOR AND NEURONAL DAMAGE IN AN
    EXPERIMENTAL MODEL OF PARKINSON'S DISEASE.
    C.W.Levenson1,2*; W.Duan2; B.Ladenheim3; R.Cutler2; M.P.Mattson2
    1. Neurosci, Florida State Univ, Tallahassee, FL, USA
    2. Lab of Neurosciences, NIA, Baltimore, MD, USA
    3. NIDA, Baltimore, MD, USA

    Because accumulation of iron in dopaminergic neurons has been
    implicated in the development of Parkinson's disease (PD), we designed
    experiments to test the impact of three levels of dietary iron in the
    pathogenic process and functional outcome in a mouse model of PD.
    Two-month-old male C57BL/6 mice were fed diets containing low (4 ppm),
    normal (48 ppm) or high (400 ppm) iron for 6 weeks prior to the
    administration of MPTP, a mitochondrial toxin that causes the death of
    nigro-striatal dopaminergic neurons and induces PD-like symptoms. As
    expected, in mice fed the normal iron diet MPTP reduced striatal
    dopamine levels and impaired motor behavior in the rotarod test
    (p<0.05). Low dietary iron increased serum total iron binding capacity
    and provided protection against the adverse effects of MPTP on motor
    function. Iron supplementation significantly impaired motor behavior
    (p<0.001) and was lethal when combined with MPTP treatment. Elevations
    of striatal 4-hydroxynonenal suggested increased membrane oxidation in
    mice fed the high iron diet. Iron treatment of cultured rat hippocampal
    neurons resulted in the generation of mitochondrial reactive oxygen
    species (ROS) that was accompanied by expression of the chaperone
    protein Hsp-70, the pro-apoptotic tumor suppressor protein p53, and
    morphological evidence of apoptosis. Furthermore, cholesterol loading
    of cells prior to iron treatment significantly increased ROS production
    and decreased cell survival suggesting that iron, cholesterol, and its
    oxidative products may act synergistically to impair neuronal survival
    in PD. In conclusion, these data suggest that dietary iron may play a
    role in the vulnerability of neurons to insults associated with PD and
    other neurodegenerative disorders.
    Support Contributed By: NIA


    Citation:
    C.W. Levenson, W. Duan, B. Ladenheim, R. Cutler, M.P. Mattson. IRON
    STATUS INFLUENCES MOTOR BEHAVIOR AND NEURONAL DAMAGE IN AN EXPERIMENTAL
    MODEL OF PARKINSON'S DISEASE. Program No. . 2003 Abstract
    Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience,
    2003. Online.

    --------------------------------------------------------------------------------

    Green tea extract 'is cancer aid'

    Green tea has been linked with a series of health benefits
    A green tea extract may help patients with a form of leukaemia, a study
    says.
    The tea, discovered in China nearly 5,000 years ago, has long been
    thought to have health benefits.

    But the team from the Mayo Clinic in the US found it appeared to
    improve the condition of four patients with chronic lymphocytic
    leukaemia (CLL).

    Experts said the Leukaemia Research journal study was interesting but
    more research was needed.

    CLL is a blood and bone marrow cancer which affects white blood cells
    and is the commonest type of leukaemia with over 3,000 new cases -
    mainly in the over 60s - diagnosed each year in the UK.

    Green tea has long been thought to have cancer-prevention
    capabilities. It is exciting that research is now demonstrating this
    agent may provide new hope for CLL patients

    Tait Shanafelt, report author

    It is called chronic leukaemia because it progresses more slowly than
    acute leukaemia with some patients living for decades with the disease.


    As their is no known cure, doctors have traditionally not intervened in
    the early stages of the disease to see how it develops, before moving
    on to traditional forms of cancer treatment such as chemotherapy.

    But the Mayo researchers decided to try green tea after a test tube
    study in 2004 showed it killed leukaemia cells.

    Four CLL patients being treated at the clinic took green tea extract
    tablets containing epigallocatechin gallate, an antioxidant thought to
    fight cancer cells.

    Doctors

    Within a few months, doctors realised that three out of four patients
    were showing signs of the cancer regressing.

    The fourth patient also showed a slight improvement, but it was not
    judged to be clinically relevant.

    Report author Tait Shanafelt said: "Green tea has long been thought to
    have cancer-prevention capabilities. It is exciting that research is
    now demonstrating this agent may provide new hope for CLL patients.

    "The experience of these individuals provides some suggestion that our
    previously published laboratory findings may actually translate into
    clinical effects for patients with this disease."

    But he warned more research was needed to prove the findings on a
    larger scaled and whether there were any side effects.

    Ken Campbell, clinical information officer at the Leukaemia Research
    Fund, said: "The findings are interesting, but we cannot say yet this
    is a new treatment for cancer.

    "We need to carry out a large scale, controlled trial to see if the
    findings hold true."

    -------------------------------------------------------------------------------------------------------------------

    <<snip>>
    may be related to both scavenger properties towards to superoxide anion
    and the ability to chelate iron ions.
    <<snip>>

    1: Planta Med. 2000 Dec;66(8):762-4. Related Articles, Links


    Protective effects of green tea catechins against asbestos-induced cell
    injury.

    Kostyuk VA, Potapovich AI, Vladykovskaya EN, Hiramatsu M.

    Green tea extract was found to provide a strong protective effect
    against asbestos-induced injury of peritoneal macrophages and red blood
    cells in vitro. The main polyphenolic constituents of green tea
    extract, (-)-epicatechin gallate (ECG) and (-)-epigallocatechin gallate
    (EGCG), were also efficient in preventing injury of cells following
    exposure to asbestos fibers. The protective efficacies of EGCG and ECG
    expressed as IC50 values were, respectively, 10 microM and 12 microM if
    peritoneal macrophages were injured by chrysotile and 4 microM and 5
    microM in the case of crocidolite-induced cell injury. Antiradical and
    chelating properties of ECG and EGCG were evaluated and it was
    concluded that the protective effect of catechins against
    asbestos-induced injury may be related to both scavenger properties
    towards to superoxide anion and the ability to chelate iron ions.

    Publication Types:
    Letter

    PMID: 11199139 [PubMed - indexed for MEDLINE]

    --------------------------------------------------------------------------------


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  2. 1: Neurosci Lett. 2005 Dec 12; [Epub ahead of print] Links


    The effect of epigallocatechin gallate on suppressing disease
    progression of ALS model mice.

    Koh SH, Lee SM, Kim HY, Lee KY, Lee YJ, Kim HT, Kim J, Kim MH, Hwang
    MS, Song C, Yang KW, Lee KW, Kim SH, Kim OH.

    Department of Neurology, Institute of Biomedical Science, College of
    Medicine, Hanyang University, #17 Haengdang-dong, Seongdong-gu, Seoul
    133-791, Republic of Korea.

    Epigallocatechin gallate (EGCG) is a constituent of green tea, and
    increasing evidence suggests that EGCG has neuroprotective effects on
    oxidative stress-injured neuronal cells, especially motoneurons.
    Although the neuroprotective effects of EGCG have been demonstrated in
    Parkinson's and Alzheimer's diseases and ischemic stroke models, there
    has been no report on the effect of EGCG on an in vivo model of
    amyotrophic lateral sclerosis (ALS). This study was undertaken to
    evaluate the effect of EGCG on ALS model mice with the human G93A
    mutated Cu/Zn-superoxide dismutase (SOD1) gene. We treated each group
    of 11 ALS model mice with EGCG (1.5, 2.9, and 5.8mug/g body weight),
    dissolved in 0.5ml of 0.9% sterile NaCl, and one group of 11 with 0.5ml
    of 0.9% sterile NaCl (control group) intraorally every day after 60
    days of age (presymptomatic treatment). The treatment of more than
    2.9mug EGCG/g body weight significantly prolonged the symptom onset and
    life span, preserved more survival signals, and attenuated death
    signals. These data suggest that EGCG could be a potential therapeutic
    candidate for ALS as a disease-modifying agent.

    PMID: 16356650 [PubMed - as supplied by publisher]

    -----------------------------------------------------------------------------


    http://www.newhopeforparkinsons.com/web/pid/98/

    By Kathrynne Holden, MS, RD

    In October 2003, Brazilian researchers published a study entitled:
    “High doses of riboflavin and the elimination of dietary red meat
    promote the recovery of some motor functions in Parkinson's disease
    patients.” Upon learning of this news, naturally many folks with PD
    wanted to know more about the diet – what foods and supplements were
    used or excluded, and whether the diet would be helpful for them. These
    are good questions and deserve a thoughtful response.

    It’s important to bear in mind that this information is based on one
    small study, and more studies are needed. Thirty-one subjects were
    enrolled, and only 19 remained for the entire six months of the study.
    Although the results are encouraging, it cannot be categorically stated
    that this plan will be helpful for everyone with PD. However, it is an
    important study and should be viewed with respect. Here are some
    reasons why:

    All of the people originally enrolled in the study were found to be
    deficient in riboflavin (vitamin B2), despite the fact that their usual
    diets contained plenty of riboflavin for normal human needs.
    All of the patients who completed six months of treatment showed
    improvement in standing, walking and balance during the first three
    months following treatment.
    About two weeks after starting the treatment regimen, many subjects
    reported better sleep at night, better reasoning ability, and less
    depression.
    How was the study conducted?

    Thirty-one people, in all stages of PD, and taking various PD
    medications or combinations of these medications, were initially
    enrolled in the study. Researchers questioned the patients about their
    usual dietary habits, and determined that their diets provided adequate
    riboflavin; also, that those with PD ate more red meat than subjects in
    a control group. Upon testing, however, they learned that all subjects
    had some degree of riboflavin deficiency.

    Because those with PD reported a higher intake of red meat, this was
    eliminated from their diet. The researchers then gave the subjects 30
    mg of riboflavin, three times daily at 8-hour intervals, a total of 90
    mg per day. The dosages were spaced throughout the day because a high
    dose of riboflavin given all at once is mostly excreted; whereas if
    given in smaller amounts throughout the day, absorption is increased.

    Twelve people dropped out of the study; 19 remained for the full six
    months. Of those remaining in the study, most reported feeling better
    after about two to three weeks. Researchers measured their motor
    capacity each month and found that they showed significant improvement
    after three months; some continued to improve throughout the length of
    the study. Riboflavin status also rose to normal levels.

    Will this diet cure Parkinson’s disease?

    No, this is not a cure for PD, and in fact, it isn’t known yet who, or
    how many, might benefit from this diet. You may want to ask your doctor
    whether this diet could be right for you.

    If new information becomes available, we will post it online on “Ask
    the Parkinson Dietitian” at www.parkinson.org.

    Here’s to your good health!

    For more on the story:
    Review the article abstract on the Ask the Parkinson Dietitian forum




    About the Author

    Ms. Holden is a registered dietitian specializing in Parkinson's
    disease. She has authored Eat Well, Stay Well with Parkinson's Disease,
    Cook Well, Stay Well with Parkinson's Disease, and Parkinson's Disease
    and Constipation. For information, see www.nutritionucanlivewith.com or
    call 877-565-2665. She moderates the e-mail forum Ask the Parkinson
    Dietitian. To join, go to: www.parkinson.org, and locate Online Forums.

    The contents of the New Hope for Parkinson's Web site and newsletter
    are for your general information only. Information you read here cannot
    replace the relationship you have with your doctor. Medtronic does not
    practice medicine or provide medical services or advice. You should
    always talk to your doctor with any questions or concerns you have
    about your general health, diagnosis or treatment.

    Health information changes quickly. Therefore, it is always best to
    confirm information with your health care professional.


    Who loves ya.
    Tom


    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
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    DEAD PEOPLE WALKING
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  3. "Low, normal, high" iron intake causes variation accordingly; which is a
    very powerful idea you are now successfully exploring. It is no longer
    "all disorders caused by iron", it is now too high iron in some contexts
    increase the risk of disorders. This is a very powerful insight you have
    made.
     
  4. Sylv

    Sylv Guest

    > It is no longer
    >"all disorders caused by iron", it is now too high iron in some contexts
    >increase the risk of disorders.


    Exactly. But I doubt Ironman understood this; concepts such as this go
    right over his head. He has been unable to understand half of what he
    posts since day one. . .

    Sylvia
     
  5. Title: Phytic acid suppresses 1-methyl-4-phenylpyridinium ion-induced
    hydroxyl radical generation in rat striatum
    Author(s): T. Obata1
    Source: Brain Research Volume: 978 Number: 1 Page: 241 -- 244
    Publisher: Elsevier Science
    Abstract:
    The present study examined the antioxidant effect of phytic acid on
    iron (II)-enhanced hydroxyl radical (*OH) generation induced by
    1-methyl-4-phenylpyridinium ion (MPP+) in the extracellular fluid of
    rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's
    solution (0.5 nmol/µl/min) was infused through a microdialysis probe to
    detect the generation of *OH as reflected by the non-enzymatic
    formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum. Phytic
    acid (100 µM) did not significantly decrease the levels of MPP+-induced
    *OH formation trapped as 2,3-DHBA. To confirm the generation of *OH by
    the Fenton-type reaction, iron (II) was infused through a microdialysis
    probe. Introduction of iron (II) (10 µM) enhanced MPP+ induced *OH
    generation. However, phytic acid significantly suppressed iron
    (II)-enhanced *OH formation after MPP+ treatment (n=6, P<0.05). These
    results suggest that the antiradical effect of phytic acid occurs by
    chelating iron required for the MPP+-enhanced *OH generation via the
    Fenton-type reaction.
    © 2003 Elsevier Science B.V., Amsterdam. All rights reserved.
    Keywords: [neuroscience society topics] Degenerative disease:
    Parkinson's; [neuroscience society topics] Disorders of the nervous
    system; Phytic acid; Fenton-type reaction; 1-Methyl-4-phenylpyridinium
    ion (MPP+); Hydroxyl radical; Parkinson's disease
    Affiliations: 1: Department of Pharmacology and Therapeutics, Oita
    Medical University, 1-1 Idaigaoka, Hasama, 879-5593, Oita, Japan




    --------------------------------------------------------------------------------


    The full text of this article is available on the Science Direct web
    site:


    --------------------------------------------------------------------------------
    © 2003 Elsevier Science B.V., Amsterdam. All rights reserved.

    Who loves ya.
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    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore


    DEAD PEOPLE WALKING
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  6. Biofactors. 2004;22(1-4):271-5. Links


    Phase 1 study of multiple biomarkers for metabolism and oxidative
    stress after one-week intake of broccoli sprouts.


    Murashima M, Watanabe S, Zhuo XG, Uehara M, Kurashige A.


    The Department of Applied Bioscience, Tokyo University of Agriculture,
    1-1-1, Sakuragaoka Setagaya, Tokyo, 156-8502, Japan. Tel.: +81 3 5477
    2453; Fax: +81 3 5477 7222; E-mail: [email protected]


    Little is known about the direct effect of broccoli sprouts on human
    health. So we investigated the effect of broccoli sprouts on the
    induction of various biochemical oxidative stress markers. Twelve
    healthy subjects (6 males and 6 females) consumed fresh broccoli
    sprouts (100 g/day) for 1 week for a phase 1 study. Before and after
    the treatment, biochemical examination was conducted and natural killer



    cell activity, plasma amino acids, plasma PCOOH (phosphatidylcholine
    hydroperoxide), the serum coenzyme Q(10), urinary 8-isoprostane, and
    urinary 8-OHdG (8-hydroxydeoxyguanosine) were measured. With treatment,



    total cholesterol and LDL cholesterol decreased, and HDL cholesterol
    increased significantly. Plasma cystine decreased significantly. All
    subjects showed reduced PCOOH, 8-isoprostane and 8-OHdG, and increased
    CoQ(10)H(2)/CoQ(10) ratio. Only one week intake of broccoli sprouts
    improved cholesterol metabolism and decreased oxidative stress markers.



    PMID: 15630296 [PubMed - in process]


    ---------------------------------------------------------------------------



    Antihypertensive Effects of Onion on NO Synthase Inhibitor-induced
    Hypertensive Rats and Spontaneously Hypertensive Rats


    Yoko SAKAI,1 Tetsuo MURAKAMI,2 and Yukiko YAMAMOTO1,


    1Graduate School of Human Life Science, Osaka City University, Sugimoto

    3-3-138, Sumiyoshi-ku, Osaka 558-8585, Japan 2Faculty of Agriculture,
    Kinki University, Nakamachi 3327-204, Nara 631-8505, Japan


    Received December 19, 2002; Accepted February 26, 2003
    This study was designed to show the effects of onion on blood pressure
    in NG-nitro-L-arginine methyl ester (L-NAME) induced-hypertensive rats
    and stroke prone spontaneously hypertensive rats (SHRSP) using dried
    onion at 5?? in their diets. For the experiment with L-NAME
    induced-hypertensive rats, male 6-weeks-old Sprague-Dawley rats were
    given tap water containing L-NAME to deliver 50 mg/kg BW/day. In this
    experiment, we found distinct antihypertensive effects of onion on the
    L-NAME induced-hypertensive rats and the SHRSP. Dietary onion decreased

    the thiobarbituric acid reactive substances (TBARS) in plasma in these
    hypertensive rats. Also, onion increased the nitrate/nitrite (products
    of nitric oxide (NO)) excreted in urine and the NO synthase (NOS)
    activity in the kidneys in SHRSP. These results suggested that the
    increased NO caused by the greater NOS activity, and additionally by
    the increased saving of NO by the antioxidative activity of onion, was
    one of the cause of the antihypertensive effect of onion in SHRSP. In
    the L-NAME induced hypertensive rats, onion did not significantly block

    the inhibition of NOS activity by L-NAME, and decreased nitrate/nitrite

    excretion in urine was not restored. The mechanism of the
    antihypertensive effect of onion probably involves increased saving of
    NO by antioxidative activity of onion in L-NAME induced-hypertensive
    rats.
    Key words: hypertension; onion; NO synthase inhibitor; SHRSP;
    antioxidant


    -17-
    ---------------------------------------------------------------------------



    Broccoli May Prevent Blindness


    Contains Antioxidant That Protects Eye Cells From UV Damage


    By Jeanie Lerche Davis
    WebMD Medical News Reviewed By Brunilda Nazario, MD
    on Tuesday, July 13, 2004


    July 13, 2004 -- To protect your eyesight, try broccoli. An antioxidant

    found
    in broccoli may be a powerful force in preventing blindness.


    Researchers at Johns Hopkins University School of Medicine have
    discovered that
    sulforaphane, the naturally occurring antioxidant in broccoli and
    broccoli
    sprouts, protects the eye from damage caused by the sun's ultraviolet
    light.


    Cells in the eye's retina are extremely sensitive to damage caused by
    oxidants,
    especially those generated by light. While several processes within the

    eye
    help cut that damage, the eye gradually loses that capability as we
    age.


    This is believed to be the primary cause of age-related macular
    degeneration --
    the leading cause of blindness, writes researcher Xiangqun Gao, a
    molecular
    scientist with the Johns Hopkins University School of Medicine. His
    report
    appears in the current issue of the Proceedings of the National Academy

    of
    Science of the USA.


    To combat this damage, a simple long-term strategy is important, Gao
    notes.
    That's where sulforaphane comes in.


    Previous studies from this group of researchers have shown that
    sulforaphane
    prevents tumor growth and kills stomach bacteria that lead to ulcers
    and
    stomach cancer. In one study, they showed that feeding broccoli sprouts

    to rats
    prevented high blood pressure, heart disease, and stroke.


    In their latest laboratory experiment, the Johns Hopkins researchers
    exposed
    human retina cells, which protect against oxidative stress and free
    radicals,
    to various doses of sulforaphane. Then they exposed cells to
    ultraviolet light
    -- similar to sunlight -- to produce oxidative damage.


    Sulforaphane protected eye cells from damage, reports Gao. In fact, the

    more
    sulforaphane exposure the cells got, the more protection they received.



    "Much evidence points to the central role of oxidative damage in
    chronic
    degenerative diseases of the eye," writes Gao. A diet high in broccoli
    and
    broccoli sprouts is a safe, long-term approach to preventing
    age-related
    macular degeneration and blindness, he says.


    --------------------------------------------------------------------------



    ------


    SOURCE: Gao, X. Proceedings of the National Academy of Science of the
    USA, July
    2004; vol 101: pp 10446-10451.


    --------------------------------------------------------------------------



    In 1992 author Steve Meyerowitz wrote that "Foods that contain
    sulforaphane a re ...
    sprouts of broccoli, kale, turnip, garlic, onion and Chinese cabbage.
    ....
    www.sproutnet.com/sprouting_seed_varieties.htm - 34k -


    --------------------------------------------------------------------------



    1: Mol Cell Biochem. 2005 Jul;275(1-2):85-94. Links


    Garlic supplementation prevents oxidative DNA damage in essential
    hypertension.


    Dhawan V, Jain S.


    Department of Experimental Medicine and Biotechnology, Research Block
    B, IInd Floor, Postgraduate Institute of Medical Education and
    Research, Chandigarh 160012, India. [email protected]


    Oxygen-free radicals and other oxygen/nitrogen species are constantly
    generated in the human body. Most are intercepted by antioxidant
    defences and perform useful metabolic roles, whereas others escape to
    damage biomolecules like DNA, lipids and proteins. Garlic has been
    shown to contain antioxidant phytochemicals that prevent oxidative
    damage. These include unique water-soluble organosulphur compounds,
    lipid-soluble organosulphur compounds and flavonoids. Therefore, in the

    present study, we have tried to explore the antioxidant effect of
    garlic supplementation on oxidative stress-induced DNA damage, nitric
    oxide (NO) and superoxide generation and on the total antioxidant
    status (TAS) in patients of essential hypertension (EH). Twenty
    patients of EH as diagnosed by JNC VI criteria (Group I) and 20 age and

    sex-matched normotensive controls (Group II) were enrolled in the
    study. Both groups were given garlic pearls (GP) in a dose of 250 mg
    per day for 2 months. Baseline samples were taken at the start of the
    study, i.e. 0 day, and thereafter 2 months follow-up.
    8-Hydroxy-2'-deoxyguanosine (8-OHdG), lipids, lipid peroxidation (MDA),

    NO and antioxidant vitamins A, E and C were determined. A moderate
    decline in blood pressure (BP) and a significant reduction in 8-OHdG,
    NO levels and lipid peroxidation were observed in Group I subjects with

    GP supplementation. Further, a significant increase in vitamin levels
    and TAS was also observed in this group as compared to the control
    subjects. These findings point out the beneficial effects of garlic
    supplementation in reducing blood pressure and counteracting oxidative
    stress, and thereby, offering cardioprotection in essential
    hypertensives.


    PMID: 16335787 [PubMed - in process]


    ---------------------------------------------------------------------------­-----



    Who loves ya.
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    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore


    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
  7. Lecithin as evidenced above leads to increased acetylcholine in the
    brain .. and again as evidenced below .. these researchers believe
    upregulation of acetylcholine in the brain is an .. anti-inflammatory
    ...


    Anti-inflammatory therapy is .. again .. recommended by the third ..
    article ..


    ---------------------------------------------------------------------------­?-----

    1: Neuropharmacology. 2005 Dec 2; [Epub ahead of print] Related
    Articles, Links

    Anti-inflammatory properties of cholinergic up-regulation: A new role
    for acetylcholinesterase inhibitors.


    Nizri E, Hamra-Amitay Y, Sicsic C, Lavon I, Brenner T.


    Laboratory of Neuroimmunology, Department of Neurology, The Agnes
    Ginges
    Center for Human Neurogenetics, Hadassah-Hebrew University Medical
    Center, P.O. Box 12000, Jerusalem 91120, Israel.


    We investigated the anti-inflammatory effects of acetylcholinesterase
    inhibitors (AChEI) at the cellular and molecular levels. AChEI
    suppressed lymphocyte proliferation and pro-inflammatory cytokine
    production, as well as extracellular esterase activity.
    Anti-inflammatory activity was mediated by the alpha7 nicotinic
    acetylcholine receptor (neuronal); the muscarinic receptor had the
    opposite effect. Treatment of the central nervous system (CNS)
    inflammatory disease, experimental autoimmune encephalomyelitis (EAE),
    with EN101, an anti-sense oligodeoxynucleotide, targeted to AChE mRNA,
    reduced the clinical severity of the disease and CNS inflammation
    intensity. The results of our experiments suggest that AChEI increase
    the concentration of extracellular acetylcholine (ACh), rendering it
    available for interaction with a nicotinic receptor expressed on
    lymphocytes. Our findings point to a novel role for AChEI which may be
    relevant in CNS inflammatory diseases such as EAE and multiple
    sclerosis. They also emphasize the importance of cholinergic balance in



    neurological disorders, such as Alzheimer's disease and myasthenia
    gravis, in which these drugs are used.


    PMID: 16336980 [PubMed - as supplied by publisher]


    ------------------------------------------------------------------------



    --------


    Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links


    Lecithin consumption raises serum-free-choline levels.


    Wurtman RJ, Hirsch MJ, Growdon JH.


    Consumption of choline by rats sequentially increases serum-choline,
    brain-choline, and brain-acetylcholine concentrations. In man
    consumption of choline increases in levels in the serum and
    cerebrospinal fluid; its administration is an effective way of treating



    tardive dyskinesia. We found that oral lecithin is considerably more
    effective in raising human serum-choline levels than an equivalent
    quantity of choline chloride. 30 minutes after ingestion of choline
    chloride (2-3 g free base), serum-choline levels rose by 86% and
    returned to normal values within 4 hours; 1 hour after lecithin
    ingestion, these levels rose by 265% and remained significantly raised
    for 12 hours. Lecithin may therefore be the method of choice for
    accelerating acetylcholine synthesis by increasing the availability of
    choline, its precursor in the blood.


    PMID: 69151 [PubMed - indexed for MEDLINE]


    ------------------------------------------------------------------------



    ---?-----
    1: Curr Med Chem. 2005;12(25):2947-62. Related Articles, Links


    Anti-inflammatory immunotherapy for multiple sclerosis/experimental
    autoimmune encephalomyelitis (EAE) disease.


    Kanwar JR.


    Department of Molecular Medicine & Pathology, Faculty of Medicine and
    Health Science, University of Auckland, Auckland, New Zealand.
    [email protected]


    Multiple sclerosis (MS) and its animal model, experimental autoimmune
    encephalomyelitis (EAE), are inflammatory diseases of the central
    nervous system (CNS) characterized by localized areas with
    demyelination. Disease is believed to be an autoimmune disorder
    mediated by activated immune cells such as T- and B-lymphocytes and
    macrophages/microglia. Lymphocytes are primed in the peripheral tissues



    by antigens, and clonally expanded cells infiltrate the CNS. They
    produce large amounts of inflammatory cytokines, nitric oxide (NO) that



    lead to demyelination and axonal degeneration. Although several studies



    have shown that oligodendrocytes (OLGs), the myelin-forming glial cells



    in the CNS, are sensitive to cell death stimuli, such as cytotoxic
    cytokines, anti-myelin antibodies, NO, and oxidative stress, in vitro,
    the mechanisms underlying injury to the OLGs in MS/EAE remain unclear.
    The central role of glutamate receptors in mediating excitotoxic
    neuronal death in stroke, epilepsy, trauma and MS has been well
    established. Glutamate is the major excitatory amino acid transmitter
    within the CNS and it's signaling is mediated by a number of
    postsynaptic ionotropic and metabotropic receptors. Inflammation can be



    blocked with anti-cell adhesion molecules MAb, simultaneously protected



    oligodendrocytes and neurons against glutamate-mediated damage with the



    AMPA/kainate antagonist NBQX, and the NMDA receptor antagonist GPE,
    could thus be effective therapies for multiple sclerosis.


    PMID: 16378498 [PubMed - in process]


    ------------------------------------------------------------------------



    --


    Who loves ya.
    Tom


    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore


    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
  8. Michael

    Michael Guest

    [email protected] wrote:

    > Lecithin as evidenced above ...



    Oh, dear.

    It seems Tom's been pushed into flood mode.

    Can you find it in your hearts to excuse him, please?

    He'll go away as soon as he feels he's victimized one or two of his imagined
    nemeses.
     
  9. Soooooo .. lefty .. what you're saying is ..

    "this thread is sht .. the studies DO NOT say .. lecithin has been
    shown in the mouse model to be MORE effective in raising acetylcholine
    in the brain. And the articles DO NOT say acetylcholine raising in the
    brain to be an intervention as an anti-inflammatory. And the articles
    DO NOT say anti-inflammatory therapy has been recommended to BE ..
    explored ..!"

    "And this article DOES NOT say .. iron targeting to be .. recommended
    ... !"

    Otherwise you are pssing on a post on a thread in MEDICAL groups ..

    Is that about .. right ..?

    Yep ..

    Nothing new for you .. eh .. lefty ..

    Heh .. heh ..

    <<snip>>
    a combination of iron chelation and antioxidant therapy might be a
    significant approach to neuroprotection neurodegenerative diseases.
    <<snip>>


    J Mol Neurosci. 2004;24(3):401-16. Links


    Iron and alpha-Synuclein in the Substantia Nigra of MPTP-Treated Mice:
    Effect of Neuroprotective Drugs R-Apomorphine and Green Tea Polyphenol
    (-)-Epigallocatechin-3-Gallate.


    Mandel S, Maor G, Youdim MB.


    Eve Topf and USA National Parkinson Foundation Centers of Excellence
    for Neurodegenerative Diseases Research and Department of Pharmacology
    and Rappaport Family Research Institute, Technion-Faculty of Medicine,
    Haifa, 31096, Israel.


    One of the prominent pathological features of Parkinson's disease (PD)
    is the abnormal accumulation of iron in the substantia nigra pars
    compacta (SNpc), in the reactive microglia, and in association with
    neuromelanin, within the melanin-containing dopamine (DA) neurons. Lewy

    body, the morphological hallmark of PD, is composed of lipids,
    redox-active iron, and aggregated alpha-synuclein, concentrating in its

    peripheral halo and ubiquitinated, hyperphosphorylated, neurofilament
    proteins. The capacity of free iron to enhance and promote the
    generation of toxic reactive oxygen radicals has been discussed
    numerous times. Recent observations, that iron induces aggregation of
    inert alpha-synuclein to toxic aggregates, have reinforced the critical

    role of iron in oxidative stress-induced pathogenesis of DA neuron
    degeneration and protein degradation via ubiquitination.
    N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- and
    6-hydroxydopamine-induced neurodegeneration in rodents and nonhuman
    primates is associated with increased presence of iron and
    alpha-synuclein in the SNpc. The accumulation of iron in MPTP-induced
    neurodegeneration has been linked to nitric oxide-dependent mechanism,
    resulting in degradation of prominent iron regulatory proteins by
    ubiquitination. Radical scavengers such as R-apomorphine and green tea
    catechin polyphenol (-)-epigallocatechin-3-gallate, as well as the
    recently developed brain-permeable VK-28 series derivative iron
    chelators, which are neuroprotective against these neurotoxins in mice
    and rats, prevent the accumulation of iron and alpha-synuclein in SNpc.

    This study supports the notion that a combination of iron chelation and

    antioxidant therapy, as emphasized on several occasions, might be a
    significant approach to neuroprotection in PD and other
    neurodegenerative diseases.


    PMID: 15655262 [PubMed - in process]


    ---------------------------------------------------------------------------­-----



    Who loves ya.
    Tom


    Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore
    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
  10. Michael

    Michael Guest

    [email protected] wrote:

    > Soooooo .. lefty .. what you're saying is ..
    >
    > "this thread is sht .. the studies DO NOT say .. lecithin has been
    > shown in the mouse model to be MORE effective in raising acetylcholine
    > in the brain. And the articles DO NOT say acetylcholine raising in the
    > brain to be an intervention as an anti-inflammatory.


    Of course they do. Don't be silly.

    Trouble is, they DO NOT say that anticholinergics produce all sorts of
    troubles of their own... which - as it happens - they do. Some of those
    troubles can be fatal.

    > And the articles
    > DO NOT say anti-inflammatory therapy has been recommended to BE ..
    > explored ..!"
    >
    > "And this article DOES NOT say .. iron targeting to be .. recommended
    > .. !"
    >
    > Otherwise you are pssing on a post on a thread in MEDICAL groups ..
    >
    > Is that about .. right ..?
    >
    > Yep ..
    >
    > Nothing new for you .. eh .. lefty ..
    >
    > Heh .. heh ..
    >
    > <<snip>>
    > a combination of iron chelation and antioxidant therapy might be a
    > significant approach to neuroprotection neurodegenerative diseases.
    > <<snip>>
    >
    >
    > J Mol Neurosci. 2004;24(3):401-16. Links
    >
    >
    > Iron and alpha-Synuclein in the Substantia Nigra of MPTP-Treated Mice:
    > Effect of Neuroprotective Drugs R-Apomorphine and Green Tea Polyphenol
    > (-)-Epigallocatechin-3-Gallate.
    >
    >
    > Mandel S, Maor G, Youdim MB.
    >
    >
    > Eve Topf and USA National Parkinson Foundation Centers of Excellence
    > for Neurodegenerative Diseases Research and Department of Pharmacology
    > and Rappaport Family Research Institute, Technion-Faculty of Medicine,
    > Haifa, 31096, Israel.
    >
    >
    > One of the prominent pathological features of Parkinson's disease (PD)
    > is the abnormal accumulation of iron in the substantia nigra pars
    > compacta (SNpc), in the reactive microglia, and in association with
    > neuromelanin, within the melanin-containing dopamine (DA) neurons.
    > Lewy
    >
    > body, the morphological hallmark of PD, is composed of lipids,
    > redox-active iron, and aggregated alpha-synuclein, concentrating in
    > its
    >
    > peripheral halo and ubiquitinated, hyperphosphorylated, neurofilament
    > proteins. The capacity of free iron to enhance and promote the
    > generation of toxic reactive oxygen radicals has been discussed
    > numerous times. Recent observations, that iron induces aggregation of
    > inert alpha-synuclein to toxic aggregates, have reinforced the
    > critical
    >
    > role of iron in oxidative stress-induced pathogenesis of DA neuron
    > degeneration and protein degradation via ubiquitination.
    > N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- and
    > 6-hydroxydopamine-induced neurodegeneration in rodents and nonhuman
    > primates is associated with increased presence of iron and
    > alpha-synuclein in the SNpc. The accumulation of iron in MPTP-induced
    > neurodegeneration has been linked to nitric oxide-dependent mechanism,
    > resulting in degradation of prominent iron regulatory proteins by
    > ubiquitination. Radical scavengers such as R-apomorphine and green tea
    > catechin polyphenol (-)-epigallocatechin-3-gallate, as well as the
    > recently developed brain-permeable VK-28 series derivative iron
    > chelators, which are neuroprotective against these neurotoxins in mice
    > and rats, prevent the accumulation of iron and alpha-synuclein in
    > SNpc.
    >
    > This study supports the notion that a combination of iron chelation
    > and
    >
    > antioxidant therapy, as emphasized on several occasions, might be a
    > significant approach to neuroprotection in PD and other
    > neurodegenerative diseases.
    >
    >
    > PMID: 15655262 [PubMed - in process]
    >
    >
    > ---------------------------------------------------------------------------­-----
    >
    >
    >
    > Who loves ya.
    > Tom
    >
    >
    > Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
    > Man Is A Herbivore!
    > http://pages.ivillage.com/ironjustice/manisaherbivore
    > DEAD PEOPLE WALKING
    > http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
  11. Sylv

    Sylv Guest

    Doughboy wrote (or attempted to write):

    >I said .. lecithin ..



    >Show me a study where .. lecithin .. >is .. 'bad' ..


    Show me. . .a post. . .where this. . .'moron'. . .
    has written a complete sentence in proper English.

    I wonder. . .what it means. . .when you. . .break up. . .sentences. .
    ..like this. Or l**ve. . .the vowels out. . .of words.

    I wonder.

    Sylvia
     
  12. I would think the least of your worries might be .. proper .. English
    ...

    I suppose proper English to YOU .. most likely .. IS .. 'more
    important' than attempting to ruuuuuun to the loo .. when you can at
    BEST .. hardly .. fkg .. walk ..

    Eh ..

    You have nothing to contribute to the thread .. stay off it ..

    Too hard for ya .. ?

    Who loves ya.
    Tom


    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore


    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
  13. Alex

    Alex Guest

    Sylv wrote:
    > Doughboy wrote (or attempted to write):
    >
    >
    >>I said .. lecithin ..

    >
    >
    >
    >>Show me a study where .. lecithin .. >is .. 'bad' ..

    >
    >
    > Show me. . .a post. . .where this. . .'moron'. . .
    > has written a complete sentence in proper English.
    >
    > I wonder. . .what it means. . .when you. . .break up. . .sentences. .
    > .like this. Or l**ve. . .the vowels out. . .of words.
    >
    > I wonder.
    >
    > Sylvia
    >


    It shows that he truly lacks even the mental capacity of his beloved
    mice to properly process the correct use of the english language. I've
    heard that lack of proper nutrition can cause that. Either that or he
    secretly lusts after Captain James T. Kirk of the Starship Enterprise.
    Hmm, maybe we should check out some of the star trek groups & see if
    he's been posting there?

    I'm still waiting to see what *his* actual contributions to science are.
    Any fool can search for keywords.

    Hey, shitstain!, what have you actually *done* to confirm any of the
    crap you post? Why haven't I seen *your* name on any of these studies?
    What's that? You don't have a lab? You don't have the mental capacity
    to reproduce the "data" you post?

    Hell, according to RustyJusty, I could google on "Nuclear Reaction
    Research" and call myself a Nuclear Researcher, right? Hmm, I could go
    by the nym "AtomicJustice", that's got a nice ring to it. Or maybe
    "AtomicAlex"! Yeah, oh wait, my family already calls me that,
    especially after I've eaten my chili. But at least it smells better
    than your "theories". Hey, we have something almost in common! Well,
    except that I only talk out my ass after eating good chili, while you
    talk out your ass constantly.

    Here's a thought, CorrosionMan, write up your resume, cite all your
    "research" experience, and try to get a job in a research lab. Don't
    forget to use all those ...'s. I hear hiring managers look for that on
    top notch resumes. Oh, and be sure to let us know how that works out
    for ya, please?

    What a maroon!

    Alex
     
  14. >>Any fool can search for keywords. <<

    Any fool can .. fk .. too ..

    It is all in .. HOW you .. fk .. buddy ..

    What part of more success in the medical field than anyone in history
    ... DON'T you understand .. ?

    You seem to be looking for something to prove your .. mettle ..?

    Explain why / how riboflavin .. seems to .. work ..

    'They' say .. "not iron binding ..!!!!! You piece of sht .. !!!"

    You must agree with them ..

    WHY does it .. work .. ?

    Step .. up ..

    You seem to think you can ..

    DOOOOOOO .. it ..

    Heh .. heh ..


    >>Why haven't I seen *your* name on any of these studies?

    What's that? You don't have a lab? You don't have the mental
    capacity
    to reproduce the "data" you post? <<

    I don't have to ..

    You see the 'key' .. is .. the work getting .. done ..

    Doesn't REALLY matter if .. I .. do it ..

    As long as it gets .. done ..

    Just because I don't have the .. ability .. TO .. 'do it myself'
    doesn't mean .. I .. didn't .. 'call it' ..

    Picolinic .. acid ..
    I called it ..
    http://tinyurl.com/d6vvz


    Anti-viral .. anti-microbial ..
    http://tinyurl.com/9hmwj


    I believe the world is .. actively looking .. for .. these .. ?

    Heh .. heh ..

    Chili .. ?
    My chili would KICK YOUR ASS ..

    And I didn't have to kill someones' .. kid ..

    Who loves ya.
    Tom


    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore


    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
  15. Michael

    Michael Guest

    [email protected] wrote:

    > My chili would KICK YOUR ASS ..
    >
    > And I didn't have to kill someones' .. kid ..


    That's stupid, Tom.

    *Everyone* knows a bit of dead kid improves the flavour of chili.
     
  16. Sylv

    Sylv Guest

    Doughboy;

    >You have nothing to contribute to the thread .. stay off it ..



    >Too hard for ya .. ?


    You have nothing useful to contribute anywhere you post. . .so you
    should just get out and stay out.

    Or is that concept over your head, too?

    Sorry, I'll try to dumb it down for you.

    Sylvia
     
  17. On 31 Dec 2005 "Sylv" <[email protected]> wrote:

    > Doughboy;
    >
    >>You have nothing to contribute to the thread .. stay off it ..

    >
    >
    >>Too hard for ya .. ?

    >
    > You have nothing useful to contribute anywhere you post. . .so you
    > should just get out and stay out.
    >
    > Or is that concept over your head, too?
    >
    > Sorry, I'll try to dumb it down for you.


    Sylvia, please don't feed a troll!

    With best wishes,

    Peter.

    --
    Peter \ / \ Prestbury, Cheltenham, Glos. GL52
    Anne \ / __ __ \ England.
    and / / \ | | |\ | / _ \ http://pnyoung.orpheusweb.co.uk
    family / \__/ \_/ | \| \__/ \______________ [email protected].
     
  18. Sylv

    Sylv Guest

    >What part of more success in the medical field than anyone in history
    >.. DON'T you understand .. ?


    BRAHAHAHAHAHAHAHA!!!! I can't stand it!

    What "success" are you talking about????

    The only "success" I have ever seen you attain is in the starting of
    flame wars on Usenet groups! Now that's a real accomplishment!

    Sylvia (who is going to be laughing over this all day)
     
  19. Sylv

    Sylv Guest

    Peter;

    > please don't feed a troll!


    I know conventional wisdom says that ignoring a troll makes it go away.
    .. .but this is not a conventional troll. I have lurked in other groups
    that he hits. Some of them are scrupulously ignoring him, but he still
    keeps coming back.

    There is a method to our madness on this group; make him go off to show
    what he really is: a nutcase. The "medical" information he posts is
    just plain useless, at best, and, at worst, it is harmful. By makiing
    him degrade into what he truly is, we are showing everyone how useless
    his "theories" are.

    People here have posted that, being new to MS, they didn't know what to
    make of him until he degenerated into his true ways. Hah! I remember
    when I used to think he knew something! I'll bet this is the case on
    other groups he plagues.

    I did hear of a lawsuit against him; some unfortunate actually took his
    advice and died of blood loss; but I have never been able to document
    this case. Google, in its infinite wisdom, has probably eradicated all
    the evidence.

    So that's why we do what we do. . .

    Sylvia
     
  20. Here is a snip from a discussion about iron in Parkinsons .. and it
    seems the Phd here .. agrees to riboflavin .. TARGETING .. iron ..

    --------------------------------------------------------------------------------------------------------
    We need to find some natural and safe substances (foods and/or
    supplements that cross the bbb) that will bind to free iron and clear
    it out of the brain. Two that I know of are green tea and lipoic acid.

    (those not interested in a bunch of chemistry should skip this
    paragraph ).

    Iron exists as either Fe(3+) or Fe(2+) and has an atomic number of 26
    (26 protons). Thus Fe(3+) has 23 electrons and 5 electrons in the outer
    shell while Fe(2+) has 24 electrons and 6 in the outer shell. So for
    the chemistry pros out there, how many electrons in the outer shell
    would be most stable for Fe? This would determine what atoms or
    molecules would bond with either Fe(3+) or Fe(2+). Such atoms or
    molecules, if they were safe to ingest and crossed the bbb, could be
    used to lower the iron levels in the brains of PWP.

    --------------------------------------------------------------------------------

    Iron chelators

    --------------------------------------------------------------------------------

    You missed out one important chelator for the excess iron we parkies
    have, that is curcumin. Not only is it anti-inflammatory, and a
    powerful antioxidant, (more so in the presence of bioperine/piperine),
    but it has a 1,3 dione structure which makes it an excellent chelator
    of excess iron.
    Ferric iron is the more stable form of iron. Ferrous iron gradually
    oxidises to ferric and remains in ferric form since it is more stable.
    Intrestingly, I think vitamin B2 (riboflavin) also forms ferric
    complexes.
    Phd


    --------------------------------------------------------------------------------

    Please explain what you mean when you say that vitamin B-2 (riboflavin)
    also forms ferric complexes.
    Is that good, or is it not?
    I know nothing about chemistry beyond glaze making for pottery! ( all
    inorganic.)
    I hope is is good since I've been taking it and pushing it vigorously
    on others here.


    --------------------------------------------------------------------------------

    It is good news, we need small amounts of iron for a stage in the
    series of reactions, converting the precursers to dopamine. However,
    Parkies tend to have an excess of iron which is a bad thing since it
    catalyses oxidation attack on the brain.
    A chemical that binds iron (or some other metals) is called a chelator,
    and vitamin B2 does this, as does curcumin. So B2 is capable of
    removing the excess of iron we have, and stops it doing any damage. B2
    therefore fastens itself to the iron forming what is known as a
    complex, and removes the excess iron from your body.
    Hope this is a clear explanation.

    Phd
    --------------------------------------------------------------------------------

    Thank you so very much for answering my question so quickly and so
    fully. That is very good to know, and it makes complete sense to me
    though I know nothing at all about organic chemistry. They really did
    do us a favor those Brazilian scientists, however faulty their study. I
    will continue taking B-2, and now I will know WHY I take it, and why it
    helps.
    All the best to you too.
    __________________

    Who loves ya.
    Tom


    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com


    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore


    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking
     
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