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1826more on how formaldehyde causes dementia -- 2013.09.24 and 2014.01.01 studies by expert teams led by Rong-Qiao He in Beijing, China: Rich Murray 2014.06.25

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  • Rich Murray
    Jun 25, 2014
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      more on how formaldehyde causes dementia -- 2013.09.24 and 2014.01.01 studies by expert teams led by Rong-Qiao He in Beijing, China: Rich Murray 2014.06.25



      J Alzheimers Dis. 2013;37(3):551-63. 
      doi: 10.3233/JAD-130602.
      Online 2013.09.24  IOS Press

      Hyperphosphorylation results in tau dysfunction in DNA folding and protection.
      Lu Y 1,
      He HJ,
      Zhou J, 
      Miao JY,
      Lu J, 
      He YG, 
      Pan R, 
      Wei Y,
      Liu Y,
      He RQ.

      Author information
      1 State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing, China 
      School of Life Science, University of Science and Technology of China, Anhui, China.

      Yang Lu 1, 2,
      Hai-Jin He 1, 
      Jun Zhou 1, 4, 
      Jun-Ye Miao 1, 4, 
      Jing Lu 1, 
      Ying-Ge He 1, 
      Rong Pan 1, 
      Yan Wei 1, 
      Ying Liu 1, 
      Rong-Qiao He 1, 3

      1 State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing, China
      2 School of Life Science, University of Science and Technology of China, Anhui, China
      3 Key Laboratory of Mental Health, Institute of Psychology, 
      Chinese Academy of Sciences, Beijing, China
      4 University of Chinese Academy of Sciences, Beijing, China

      Abstract

      Hyperphosphorylation of tau occurs in preclinical and clinical stages of Alzheimer's disease (AD), and hyperphosphorylated tau is the main constituent of the paired helical filaments in the brains of mild cognitive impairment and AD patients. 

      While most of the work described so far focused on the relationship between hyperphosphorylation of tau and microtubule disassembly as well as axonal transport impairments, both phenomena ultimately leading to cell death, little work has been done to study the correlation between tau hyperphosphorylation and DNA damage.

      As we showed in this study, tau hyperphosphorylation and DNA damage co-occurred under formaldehyde treatment in N2a cells, indicating that phosphorylated tau (p-Tau) induced by formaldehyde may be involved in DNA impairment. 

      After phosphorylation, the effect of tau in preventing DNA from thermal denaturation was diminished, its ability to accelerate DNA renaturation was lost, and its function in protecting DNA from reactive oxygen species (ROS) attack was impaired.

      Thus, p-Tau is not only associated with the disassembly of the microtubule system, but also plays a crucial role in DNA impairment. 

      Hyperphosphorylation-mediated dysfunction of tau protein in prevention of DNA structure from damage under the attack of ROS may provide novel insights into the mechanisms underlying tauopathies.

      PMID: 24064506




      J Alzheimers Dis. 2014 Jan 1;40(4):1039-53.
      doi: 10.3233/JAD-131595.
      Online 2014.02.28  IOS Press

      A Novel Mechanism for Endogenous Formaldehyde Elevation in SAMP8 Mouse.
      Qiang M 1,
      Xiao R 2, 
      Su T 1, 
      Wu BB 3,
      Tong ZQ 3, 
      Liu Y 3, 
      He RQ 4.

      Min Qiang 1, 3,
      Rong Xiao 1, 4, 
      Tao Su 1, 3, 
      Bei-Bei Wu 1, 
      Zhi-Qian Tong 1, 
      Ying Liu 1, 
      Rong-Qiao He 1, 2

      Author information
      1 State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing, 
      China University of Chinese Academy of Sciences, Beijing, China.
      2 State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing, China 
      School of Life Science, Liaoning Normal University, Dalian, China.
      3 State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing, China.
      4 State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, 
      Chinese Academy of Sciences, Beijing, China
      Key Laboratory of Mental Health, Institute of Psychology,
      Chinese Academy of Sciences, Beijing, China.

      Abstract

      Alzheimer's disease (AD) is the most common form of dementia, affecting millions of people worldwide.
       
      Increasing evidence suggests that formaldehyde might be one of the various pathological mechanisms involved in the process of AD onset.

      Here, we use an AD mouse model, senescence accelerated mouse-prone 8 strain (SAMP8), to study the relationship between endogenous formaldehyde and impairment of cognition.

      The Morris water maze test was used to evaluate the spatial learning and memory ability of 3-month-old SAMP8 mice, and we correlated the results with endogenous formaldehyde concentrations in the brain. 

      To investigate the underlying reasons for formaldehyde elevation in neurodegenerative diseases, the expression levels of enzymes involved in formaldehyde metabolism were analyzed, including (anabolic) semicarbazide sensitive amine oxidase (SSAO) and (catabolic) alcohol dehydrogenase III (ADH3). 

      When compared with age-matched SAMR1 mice, we found that in 3-month-old SAMP8 mice the capacity for spatial learning and memory was lower, while brain formaldehyde levels were higher.

      By using real-time PCR, western blotting, enzyme assay, and immunohistochemistry techniques, we discovered that SSAO expression levels were increased, whereas ADH3 exhibited reduced expression levels of mRNA, protein, and enzyme activity.

      The imbalance of these metabolic enzymes may represent a causal explanation for the observed formaldehyde elevation in the SAMP8 brain. 

      Such increase could be responsible for the observed tau hyperphosphorylation assumed to result in protein aggregation, ultimately leading to cognitive impairment. 

      Taken together, our study gives new insights into the role of metabolic enzymes in age-related accumulation of formaldehyde, and thus the establishment of neurodegenerative diseases.

      KEYWORDS:
      ADH3; Alzheimer's disease; SAMP8; SAMR1; SSAO; enzymes; formaldehyde; metabolism

      PMID: 24583407



      two studies by Rong-Qiao He teams in China on monkeys and mice show oral methanol leads to specific formaldehyde harm similar to Alzheimers disease, confirming WC Monte paradigm: Rich Murray 2014.05.16


      Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004, on  WhileScienceSleeps.com  gives free bibliography of 782 mostly full text medical research papers.

      While Science Sleeps shared a link.
      May 8 2014


      Two new studies fully support Prof. Monte's assertions regarding the link between Aspartame and Alzheimer's Disease:



      From Prof. Monte:

      "These scientists from the most prestigious of the national Chinese neurological laboratories have now shown that the "only" reliable and human reflective animal model Alzheimer's that causes both anatomical signs of the disease (Tau agglomeration and plaque formation) is to feed monkeys methanol.......The unauthorized 30 year study done in the United States on unknowing humans is ongoing and has shown that the methanol from aspartame has increased incidence of Alzheimer in the human population by 100 times.......and climbing."



      J Alzheimers Dis. 2014 Apr 30. [Epub ahead of print]

      Alzheimer's Disease and Methanol Toxicity (Part 2): Lessons from Four Rhesus Macaques (Macaca mulatta) Chronically Fed Methanol.

      Yang M 1, 
      Miao J 2,
      Rizak J 1,
      Zhai R 1,
      Wang Z 3,
      Anwar TH 3,
      Li T 2, 
      Zheng N 1,
      Wu S 1, 
      Zheng Y 3,
      Fan X 3, 
      Yang J 3,
      Wang J 3, 
      Ma Y 4,
      Lü L 5, 
      He R 6,
      Hu X 7.

      Meifeng Yang 1, 3,
      Junye Miao 2, 3,
      Joshua Rizak 1, 3, 
      Rongwei Zhai 1, 3, 
      Zhengbo Wang 1, 
      Tanzeel Huma Anwar 1, 
      Ting Li 2, 3,
      Na Zheng 1, 3,
      Shihao Wu 1, 3,
      Yingwei Zheng 1, 
      Xiaona Fan 1, 
      Jianzhen Yang 1,
      Jianhong Wang 1, 
      Yuanye Ma 1, 2, 5, 
      Longbao Lü 4, 
      Rongqiao He 2   Rong-Qiao He  <herq@...>, 
      Xintian Hu 1, 5

      Author information

      1 State Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, 
      Chinese Academy of Sciences, Kunming, Yunnan, P.R. China 
      University of the Chinese Academy of Science, Beijing, P.R. China.

      2 State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, 
      Chinese Academy of Sciences, Beijing, P.R. China
      University of the Chinese Academy of Science, Beijing, P.R. China.

      3 State Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology,
      Chinese Academy of Sciences, Kunming, Yunnan, P.R. China.

      4 State Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology,
      Chinese Academy of Sciences, Kunming, Yunnan, P.R. China
      State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing, P.R. China
      Yunnan Key Laboratory of Primate Biomedical Research, Kunming, Yunnan, China.

      5 Kunming Primate Research Center of the Chinese Academy of Sciences,
      Kunming Institute of Zoology, 
      Chinese Academy of Sciences, Kunming, Yunnan, P.R. China.

      6 State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, 
      Chinese Academy of Sciences, Beijing, P.R. China.

      7 State Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, 
      Chinese Academy of Sciences, Kunming, Yunnan, P.R. China 
      Yunnan Key Laboratory of Primate Biomedical Research, Kunming, Yunnan, China.

      Abstract

      A recently established link between formaldehyde, a methanol metabolite, and Alzheimer's disease (AD) pathology has provided a new impetus to investigate the chronic effects of methanol exposure.

      This paper expands this investigation to the non-human primate, rhesus macaque, through the chronic feeding of young male monkeys with 3% methanol ad libitum. 

      Variable Spatial Delay Response Tasks of the monkeys found that the methanol feeding led to persistent memory decline in the monkeys that lasted 6 months beyond the feeding regimen.

      This change coincided with increases in tau protein phosphorylation at residues T181 and S396 in cerebrospinal fluid during feeding as well as with increases in tau phosphorylated aggregates and amyloid plaques in four brain regions postmortem: 
      the frontal lobe, 
      parietal lobe,
       temporal lobe,
      and the hippocampus.

      Tau phosphorylation in cerebrospinal fluid was found to be dependent on methanol feeding status, but phosphorylation changes in the brain were found to be persistent 6 months after the methanol feeding stopped.
       
      This suggested the methanol feeding caused long-lasting and persistent pathological changes that were related to AD development in the monkey. 

      Most notably, the presence of amyloid plaque formations in the monkeys highlighted a marked difference in animal systems used in AD investigations, suggesting that the innate defenses in mice against methanol toxicity may have limited previous investigations into AD pathology.

      Nonetheless, these findings support a growing body of evidence that links methanol and its metabolite formaldehyde to AD pathology.

      KEYWORDS:

      Alzheimer's disease, amyloid plaque formation, cognitive impairment, disease progression, formaldehyde, methanol toxicity, tau hyperphosphorylation

      PMID: 24787917




      Alzheimer's Disease and Methanol Toxicity (Part 1): Chronic Methanol Feeding Led to Memory Impairments and Tau Hyperphosphorylation in Mice

      Journal Journal of Alzheimer's Disease
      Publisher IOS Press
      ISSN 1387-2877 (Print)
      1875-8908 (Online)
      Subject Medicine, Clinical Neurology and Internal Medicine
      Pages -
      DOI 10.3233/JAD-131529
      Subject Group Medicine and Health
      Online Date Wednesday, April 30, 2014

      Meifeng Yang 2, 3, 
      Jing Lu 1, 3, 
      Junye Miao 1, 3,
      Joshua Rizak 2, 
      Jianzhen Yang 2, 
      Rongwei Zhai 2, 3,
      Jun Zhou 1, 3, 
      Jiagui Qu 2, 
      Jianhong Wang 2,
      Yuanye Ma 1, 2, 4, 
      Xintian Hu 2, 4, 
      Rongqiao He 1  Rong-Qiao He  <herq@...>,


      1 State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, 
      Chinese Academy of Sciences, Beijing, P.R. China

      2 State Key Laboratory of Animal Models and Human Disease Mechanisms, 
      Chinese Academy of Sciences, 
      Kunming Institute of Zoology, Kunming, Yunnan, P.R. China

      3 University of the Chinese Academy of Science, Beijing, P.R. China

      4 Yunnan Key Laboratory of Primate Biomedical Research, Kunming, Yunnan, P.R. China


      Abstract

      Although methanol toxicity is well known for acute neurological sequelae leading to blindness or death, there is a new impetus to investigate the chronic effects of methanol exposure.

      These include a recently established link between formaldehyde, a methanol metabolite, and Alzheimer's disease (AD) pathology.

      In the present study, mice were fed with methanol to revisit the chronic effects of methanol toxicity, especially as it pertains to AD progression.

      Three groups of mice (n = 9) were given either water as a control or a methanol solution (concentrations of 2% or 3.8%) over a 6-week period. 

      The methanol-fed mice were found to have impaired spatial recognition and olfactory memory in Y-maze and olfactory memory paradigms.

      Immunohistochemical analysis of the mouse brains found increased neuronal tau phosphorylation in the hippocampus and an increased cellular apoptotic marker in hippocampal CA1 neurons (~10% of neurons displayed chromatin condensation) in the methanol-fed groups. 

      Two additional in vitro experiments in mouse embryonic cerebral cortex neurons and mouse neuroblastoma N2a cells found that formaldehyde,
      but not methanol or the methanol end product formic acid, 
      induced microtubule disintegration and tau protein hyperphosphorylation. 

      The findings of the behavioral tests and immunohistochemical analysis suggested that the methanol-fed mice presented with partial AD-like symptoms.

      The in vitro experiments suggested that formaldehyde was most likely the detrimental component of methanol toxicity related to hippocampal tau phosphorylation and the subsequent impaired memory in the mice. 

      These findings add to a growing body of evidence that links formaldehyde to AD pathology.

      Keywords

      Alzheimer's disease, cognitive impairment, disease progression, formaldehyde, methanol, tau hyperphosphorylation



      Rong-Qiao He team -- many studies on formaldehyde harm to tau protein in Alzheimer's Disease -- WC Monte paradigm shows methanol is made into formaldehyde inside human cells by ADH1 enzyme: Rich Murray 2013.05.08




      Biochim Biophys Acta. 2013 Apr 28.
      pii: S0304-4165(13)00168-2.
      doi: 10.1016/j.bbagen.2013.04.028.
      [Epub ahead of print]
      Formaldehyde induces hyperphosphorylation and polymerization of Tau protein both in vitro and in vivo.
      Lu J,
      Miao J,
      Su T, 
      Liu Y,
      He R.
      State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing 100101, China;
      University of Chinese Academy of Sciences, Beijing 100049, China;
      The University of Queensland, Queensland Brain Institute, Qld 4072, Australia.

      Highlights

      * Formaldehyde can induce hyperphosphorylation of Tau protein in both N2a cells and mouse brain.

      * Hyperphosphorylated Tau induced by formaldehyde occurs not only in cytoplasm but also in nucleus of cell.

      * GSK-3β is involved in the formaldehyde-induced hyperphosphorylation of Tau.

      * Hyperphosphorylated Tau induced by formaldehyde forms ThS-positive polymers in cells.

      Abstract

      BACKGROUND:
      Chronic formaldehyde exposure leads to memory impairment and abnormal elevation of endogenous formaldehyde has been found in the brains of Alzheimer's disease (AD) patients.

      Hyperphosphorylated Tau protein with subsequent aggregates as neurofibrillary tangles (NFTs) is one of the typical pathological characteristics in AD brains.

      The mechanism underlying abnormally elevated concentrations of endogenous formaldehyde that induce Tau hyperphosphorylation is unknown.

      METHODS:
      N2a cells and mice were treated with formaldehyde for different time points, then Western blotting and immunocytochemistry were utilized to determine the phosphorylation and polymerization of Tau protein. 

      HPLC was used to detect the concentration of formaldehyde in cell media.

      RESULTS:
      Under formaldehyde stress, Tau became hyperphosphorylated, not only in the cytoplasm, but also in the nucleus of neuroblastoma (N2a) cells, and mouse brains. 

      Polymers of cellular phospho-Tau were also detected.

      Significant accumulation of glycogen synthase kinase-3β (GSK-3β) in the nucleus of N2a and mouse brain cells, and elevation of its phosphorylation at Y216, was observed under formaldehyde stress.

      Formaldehyde-induced Tau hyperphosphorylation was blocked in the presence of LiCl and CT99021, inhibitors of GSK-3β, and by RNAi interference.

      CONCLUSIONS:
      Formaldehyde, which may cause age-related memory loss, can act as a factor triggering Tau hyperphosphorylation via GSK-3β catalysis and induces polymerization of Tau.

      GENERAL SIGNIFICANCE:
      Investigation of formaldehyde-induced Tau hyperphosphorylation may provide novel insights into mechanisms underlying tauopathies.
      [ i.e., Alzheimer's Disease ]

      Copyright © 2013. Published by Elsevier B.V.

      PMID: 23628704

      Jing Lu a, c, d, 1,
      Junye Miao a, c, 1, 
      Tao Su a, c,
      Ying Liu a,
      Rongqiao He a, b,    Rong-Qiao He  <herq@...>, 

      a State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics,
      Chinese Academy of Sciences, Beijing 100101, China
      b Key Laboratory of Mental Health, Institute of Psychology,
      Chinese Academy of Sciences, Beijing 100101, China
      c University of Chinese Academy of Sciences, Beijing 100049, China
      d The University of Queensland, Queensland Brain Institute, Qld 4072, Australia

      Abbreviations:

      AD, Alzheimer's disease;
      GSK-3β, glycogen synthase kinase-3β;
      NFTs, neurofibrillary tangles;
      PHFs, paired helical filaments;
      FA, formaldehyde;
      pTau, phosphorylated Tau

      Keywords:

      Formaldehyde; Tau hyperphosphorylation; GSK-3β; Nuclear accumulation; Protein polymerization; Tauopathy



      Annlia Paganini Hill <apaganin@...>

      ethanol is a potent antidote that in humans prevents ADH1 enzyme from making methanol (wood alcohol) from being made into formaldehyde right inside cells of 20 tissues, WC Monte paradigm: Rich Murray 2014.05.05

      Claudia H. Kawas <ckawas@...


      "People who drank moderate amounts of alcohol or coffee lived longer than those who abstained."

      See more at:


      methanol from aspartame, cigarette and wood smoke, unfresh fruits is made in humans only by ADH1 enzyme into formaldehyde inside cells of 20 tissues, causing much random methylation of DNA --  WC Monte paradigm has 782 free full text references: Rich Murray 2014.05.05


      about half of diet sodas use aspartame, 22 mg methanol per can, made by ADH1 enzyme into formaldehyde right inside cells of 20 human tissues, including inner walls of blood vessels, methanol also in cigarette smoke and unfresh fruits and juices sealed in jars, WC Monte gives 782 free full text references at WhileScienceSleeps.com: Ankur Vyas: Rich Murray 2014.04.16


      UI study finds diet drinks associated with heart trouble for older women
      Iowa Now -- The University of Iowa



      aspartame 250 (methanol 27.5) mg per kg bw oral daily for 60 days in rats causes severe nerve harm in Purkinje cells -- ADH1 enzyme makes methanol into formaldehyde inside Purkinje cells -- WC Monte paradigm: Rich Murray 2014.04.13


      Esteemed Manal Abdul-Hamid and  Sanaa Rida Gallaly:

      Your results confirm a key point in the new paradigm for methanol-formaldehyde toxicity given since fall, 2007 by Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004, on his website WhileScienceSleeps.com , supported  by a free online archive of 782 mostly full text medical research reports.

      Ethanol (ordinary drinking alcohol) at low blood levels preoccupies the ADH1 enzyme, and so is also a very potent antidote, used by hospitals in human cases of acute methanol toxicity to prevent the formation of formaldehyde from methanol -- this treatment quickly ends the ongoing harm, until the methanol gradually leaves the blood with a half-life of 3 hours in humans for several days.

      within the fellowship of service,  Rich Murray


      Ultrastruct Pathol. 2014 Mar 31. [Epub ahead of print]
      Ameliorative Effect of Pimpinella anisum Oil on Immunohistochemical and Ultrastructural Changes of Cerebellum of Albino Rats Induced by Aspartame.
      Abdul-Hamid M 1, Gallaly SR.
      Author information
      1 Department of Zoology, Faculty of Science,
      Beni-Suef University , Beni Suef , Egypt.


      Posted online on March 31, 2014. (doi:10.3109/01913123.2014.889259)
      HTML
      PDF (2127 KB)
      PDF Plus (2127 KB)

      Manal Abdul-Hamid, PhD <medo_bio@...>
      and Sanaa Rida Gallaly, PhD
      Department of Zoology, Faculty of Science, 
      Beni-Suef University, Beni Suef, Egypt

      Correspondence: 
      Manal Abdul-Hamid, Ass. Prof. of Histology and Cytology,
      Department of Zoology, Faculty of Science, 
      Beni-Suef University, Beni Suef 62511, Egypt.
      E-mail: medo_bio@...

      Abstract

      The study aims to investigate the protective effect of Pimpinella anisum oil on aspartame (ASP) which resulted in cerebellar changes.

      The rats were divided into four equal groups:

      Group 1: (control group): served as control animals.

      Group 2: control P. anisum oil received .5 mL/kg/d/b wt. once daily.

      Group 3 (ASP group): received daily 250 mg/kg/b wt. of ASP dissolved in distilled water and given orally to the animals by intra-gastric tube for 2 months.

      Group 4: received .5 mL/kg/b wt. of prophylactic P. anisum oil once daily,
      followed by ASP after 2 h for 2 months. 

      The histopathological approach revealed marked changes in the Purkinje cells, myleinated nerve fibers and granular cells of ASP-treated animals. 

      Some of these cells appeared with deeply stained cytoplasm. 

      Ultrastructural examination showed Purkinje cells with dilated rough endoplasmic reticulum and condensed mitochondria. 

      Granular cells appeared with less c nuclei and surrounded by dissolution of most Mossy rosettes structures. 

      Most myelinated nerve fibers showed thickening of myelinated sheath and others showed splitting of their myelin sheath. 

      The histopathological, immunohistochemical and ultrastructural alterations were much less observed in concomitant use of P. anisum oil with ASP. 

      Cerebellar cortex is considered target areas of ASP neurotoxicity, while P. anisum oil, when used in combination with ASP displays a protective action against neurotoxicity.

      PMID: 24684500



      methanol from cigarette and wood smoke, aspartame, canned fruits -- made into formaldehyde by ADH1 enzyme in islets of Langerhans in pancreas -- causes epigenetic changes in diabetes 2 -- WC Monte paradigm: Rich Murray 2014.03.10



      free full text

      Editor: 
      John M. Greally, Albert Einstein College of Medicine, United States of America

      Received:
      July 20, 2013; Accepted: December 20, 2013; Published: March 6, 2014

      Tasnim Dayeh <Tasnim.Dayeh@...>,
      Petr Volkov,
      Sofia Salö,
      Elin Hall, 
      Emma Nilsson,
      Anders H. Olsson,
      Clare L. Kirkpatrick, 
      Claes B. Wollheim, 
      Lena Eliasson,
      Tina Rönn, 
      Karl Bacos,
      Charlotte Ling <charlotte.ling@...>,

      Genome-Wide DNA Methylation Analysis of Human Pancreatic Islets from Type 2 Diabetic and Non-Diabetic Donors Identifies Candidate Genes That Influence Insulin Secretion. 

      PLoS Genetics, 2014; 10 (3): e1004160
      DOI: 10.1371/journal.pgen.1004160




      Methyl alcohol ingestion as a model etiologic agent in multiple
      sclerosis, WC Monte, D Glanzman, C Johnston; Methanol induced
      neuropathology in the mammalian central nervous system, Woodrow C.
      Monte, Renee Ann Zeising, both reports 1989.12.04: Murray 2007.12.28
      2012.05.01


      Aspartame: The hidden danger [methanol/formaldehyde] in our midst and
      how it kills us, 12 page review of While Science Sleeps text (Woodrow
      C Monte), International Health News, whole June issue, Editor: William
      R Ware PhD: Rich Murray 2012.06.08

      [ much more... ]


      careful expert lifetime study on mice shows liver and lung cancers
      from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
      by US National Toxicology Program experts, confirms many previous
      studies from 2001 on: Rich Murray 2011.02.27
      http://rmforall.blogspot.com/ 2011/02/careful-expert- lifetime-study-on-mice.html
      http://health.groups.yahoo. com/group/aspartameNM/message/ 1619



      Prof. Erik Millstone 2013.12.16 crisp critique of EFSA blatant pro-industry bias on 2013.12.10 aspartame decision --  Sepp Hasslberger blog: Rich Murray 2014.01.07
      http://rmforall.blogspot.com/ 2014/01/prof-erik-millstone- 20131216-crisp.html


      research on aspartame (methanol, formaldehyde, formic acid) toxicity: Rich Murray 2004.07.11 2014.01.21
      http://rmforall.blogspot.com/ 2014/01/research-on-aspartame- methanol.html
      http://groups.yahoo.com/group/ aspartameNM/message/1806 part 1 of 2
      http://groups.yahoo.com/group/ aspartameNM/message/1809 part 2 of 2
      http://groups.yahoo.com/group/ aspartameNM/message/1100  original


      "As a matter of course, every soul citizen of Earth has a priority to quickly find and positively share evidence for healthy and safe food, drink, environment, and society."

      within the fellowship of service,

      Rich Murray,
      MA Boston University Graduate School 1967 psychology,
      BS MIT 1964 history and physics,
      1039 Emory Street, Imperial Beach, CA 91932