I take green/white tea and EGCG supplements with my Zocor
Posted: Sun Mar 02, 2014 7:58 pm
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http://home.ix.netcom.com/~jdalton/egcg-neorond-ms.pdf
jackD
I would have just posted the Abstracts but they are useless!!! These guys have "novel" brains!!!
1. J Neuroimmunol. 2007 Mar;184(1-2):17-26. Epub 2007 Jan 10.
Neurodegeneration in autoimmune demyelination: recent mechanistic insights reveal novel therapeutic targets.
Aktas O1, Waiczies S, Zipp F.
Author information:
1Institute for Neuroimmunology, Neuroscience Research Center, Charité -- Universitätsmedizin Berlin, Germany.
Abstract
Multiple sclerosis (MS) is the most common chronic demyelinating disease of the central nervous system (CNS) and the major cause of neurological disability in young adults in Western countries. In spite of intensive research efforts, treatment options established to date do not sufficiently prevent the accumulation of tissue damage and clinical disability in patients with MS. We here describe recently identified molecules responsible for the inflammatory and the neurodegenerative processes in MS and its animal model, experimental autoimmune encephalomyelitis (EAE), and review new treatment options targeting both aspects of this disease.
PMID: 17222462 [PubMed - indexed for MEDLINE]
1. J Neuroimmunol. 2007 Mar;184(1-2):27-36. Epub 2006 Dec 26.
Neurodegeneration and -protection in autoimmune CNS inflammation.
Diem R1, Sättler MB, Bähr M.
Author information:
1Neurologische Universitätsklinik, Robert-Koch-Str. 40, D-37075 Göttingen, Germany.
Abstract
Neurodegeneration in multiple sclerosis (MS) is the structural correlate of permanent neurological disability in patients. The histopathological features of neurodegeneration include destruction of axons as well as apoptotic cell death of neuronal cell bodies. Therapeutic efforts to control these clinically important aspects of MS pathology showed limited success so far. In this review article, we give an overview about the current knowledge concerning the molecular mechanisms of neurodegeneration in autoimmune inflammation that is mainly derived from animal models. Further, we critically discuss experimental neuroprotective strategies with respect to their functional relevance and differentiate between anti-apoptotic and axon protective treatment approaches.
PMID: 17188756 [PubMed - indexed for MEDLINE]
http://home.ix.netcom.com/~jdalton/egcg-neorond-ms.pdf
jackD
I would have just posted the Abstracts but they are useless!!! These guys have "novel" brains!!!
1. J Neuroimmunol. 2007 Mar;184(1-2):17-26. Epub 2007 Jan 10.
Neurodegeneration in autoimmune demyelination: recent mechanistic insights reveal novel therapeutic targets.
Aktas O1, Waiczies S, Zipp F.
Author information:
1Institute for Neuroimmunology, Neuroscience Research Center, Charité -- Universitätsmedizin Berlin, Germany.
Abstract
Multiple sclerosis (MS) is the most common chronic demyelinating disease of the central nervous system (CNS) and the major cause of neurological disability in young adults in Western countries. In spite of intensive research efforts, treatment options established to date do not sufficiently prevent the accumulation of tissue damage and clinical disability in patients with MS. We here describe recently identified molecules responsible for the inflammatory and the neurodegenerative processes in MS and its animal model, experimental autoimmune encephalomyelitis (EAE), and review new treatment options targeting both aspects of this disease.
PMID: 17222462 [PubMed - indexed for MEDLINE]
1. J Neuroimmunol. 2007 Mar;184(1-2):27-36. Epub 2006 Dec 26.
Neurodegeneration and -protection in autoimmune CNS inflammation.
Diem R1, Sättler MB, Bähr M.
Author information:
1Neurologische Universitätsklinik, Robert-Koch-Str. 40, D-37075 Göttingen, Germany.
Abstract
Neurodegeneration in multiple sclerosis (MS) is the structural correlate of permanent neurological disability in patients. The histopathological features of neurodegeneration include destruction of axons as well as apoptotic cell death of neuronal cell bodies. Therapeutic efforts to control these clinically important aspects of MS pathology showed limited success so far. In this review article, we give an overview about the current knowledge concerning the molecular mechanisms of neurodegeneration in autoimmune inflammation that is mainly derived from animal models. Further, we critically discuss experimental neuroprotective strategies with respect to their functional relevance and differentiate between anti-apoptotic and axon protective treatment approaches.
PMID: 17188756 [PubMed - indexed for MEDLINE]