Elevated Iron and ALS
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From: ironjustice on 6 Aug 2008 10:38 "General increase in stored iron" Increased serum ferritin levels in amyotrophic lateral sclerosis (ALS) patients. J Neurol. 2008 Jul 18. Goodall EF, Haque MS, Morrison KE. Molecular Neurology Group, Division of Neuroscience, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK. Iron misregulation promotes oxidative stress, a proposed pathological mechanism in neurodegenerative disease. The aim of this study was to evaluate serum iron metabolism indicators in 60 amyotrophic lateral sclerosis (ALS) patients and 44 age matched controls. Serum ferritin levels were significantly increased in ALS patients compared to controls (p < 0.001), while no differences in the levels of serum iron, transferrin, iron saturation or total iron binding capacity were found. Likewise no differences in C reactive protein (CRP) or caeruloplasmin were detected, suggesting that the elevated ferritin levels in ALS did not merely indicate an acute phase response. The increased ferritin level may reflect a general increase in stored iron or be a consequence of ongoing muscle degeneration. PMID: 18677636 Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
From: RtecMontee on 6 Aug 2008 20:49 "Magnet treatment" ! <ironjustice(a)aol.com> wrote in message news:88a8c288-437a-4100-a703-a492bceeed05(a)56g2000hsm.googlegroups.com... "General increase in stored iron" Increased serum ferritin levels in amyotrophic lateral sclerosis (ALS) patients. J Neurol. 2008 Jul 18. Goodall EF, Haque MS, Morrison KE. Molecular Neurology Group, Division of Neuroscience, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK. Iron misregulation promotes oxidative stress, a proposed pathological mechanism in neurodegenerative disease. The aim of this study was to evaluate serum iron metabolism indicators in 60 amyotrophic lateral sclerosis (ALS) patients and 44 age matched controls. Serum ferritin levels were significantly increased in ALS patients compared to controls (p < 0.001), while no differences in the levels of serum iron, transferrin, iron saturation or total iron binding capacity were found. Likewise no differences in C reactive protein (CRP) or caeruloplasmin were detected, suggesting that the elevated ferritin levels in ALS did not merely indicate an acute phase response. The increased ferritin level may reflect a general increase in stored iron or be a consequence of ongoing muscle degeneration. PMID: 18677636 Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
From: jay on 7 Aug 2008 21:03
> Increased serum ferritin levels in amyotrophic lateral sclerosis (ALS) > patients. > Iron misregulation promotes oxidative stress, a proposed pathological > mechanism in neurodegenerative disease. Th increased ferritin > level may reflect a general increase in stored iron > or be a consequence of ongoing muscle degeneration. > PMID: 18677636 Even while POPs in dietary fats are decreasing, due to TCDD's long half life (10 years), it is still increasing in most people's fatty tissue, which includes the nervous system. TCDD causes cells to absorb additional iron in order to form detox enzymes which results in increased free radicals and in some cases damaged DNA. Histologic evidence for a toxic polyneuropathy due to exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rats. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a considerable environmental hazard in industrial societies. Its toxic effects on animals and humans are numerous, but little is known about its neurotoxicity. We studied the neurotoxic effects of TCDD in 80 male, adult Wistar rats. The substance was dissolved in corn oil and a single dose injected intraperitoneally (8.8 micrograms, 6.6 micrograms, 4.4 micrograms or 2.2 micrograms/kg). Neurophysiological examinations proved a dose-related, statistically significant slowing of sensory and motor conduction velocities. Ten months after the application of TCDD peripheral nerves showed a progressive, and proximally accentuated neuropathy. The extent of changes, however, differed remarkably between individual animals. Our data indicate that TCDD caused a toxic polyneuropathy in rats. PMID: 8296535 Neurotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in cerebellar granule cells. Environmental pollutant, tetrachloro dibenzo dioxin (TCDD) is known to illicit the cognitive disability and motor dysfunction in the developing brain. TCDD induced effects leading to neurodevelopmental and neurobehavioral deficit may have been defined, however underlying molecular mechanism and possible intracellular targets remain to be elucidated. In this study, we attempted to analyze TCDD-induced neurotoxic effects in the granule cells from cerebellum where certain cognitive abilities and motor function command are known to be excuted .... Vitamin E attenuated the TCDD-induced ROS production indicating that TCDD-induced ROS formation may be associated with activation of ERK-1/2 in the MAP kinase pathway or the NMDA receptor. TCDD also increased [Ca2+]i, which is associated with ROS formation and PKC activation in the cerebellar granule cells. It is suggested that TCDD activates the NMDA receptor, which may induce a sustained increase of [Ca2+]i in neurons followed by the ROS formation. Our findings may contribute to understanding the mechanism of TCDD-related neurotoxicity, thereby improving the health risk assessment of neurotoxic compounds in humans. PMID: 15761253 |