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.
1Institute for Neuroimmunology, Neuroscience Research Center, Charité -- Universitätsmedizin Berlin, Germany.
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.
1Neurologische Universitätsklinik, Robert-Koch-Str. 40, D-37075 Göttingen, Germany.
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]
This does require you to believe that MS is a two stage disease.Targeting the different levels of inflammatory neurodegeneration. Our current understanding of autoimmune demyelination imparts the necessity for therapeutic approaches to target inflammation and neurodegeneration simultaneously. This can be achieved by applying molecules which are capable of targeting both pathogenetic processes or by applying combination therapies. While targeting TRAIL signaling in the CNS offers therapeutic benefit for T cell-mediated neuronal damage, targeting the HMGCR pathway is more likely to keep the immune response under control. By targeting the proteosome with polyphenols such as EGCG, therapeutic benefit is rendered for both inflammation and neuronal damage altogether.]
So I take my Zocor with my mega dose of green tea extract(EGCGs) each night. It works!!
p.s. Of course some will note that it was just a small study base upon a small population and that the results may be different if a larger sample population is used in future studies.
p.p.s. The only thing worse than high dose Lipitor is high dose Zocor.
BMC Med. 2007 Jul 19;5:20.
Simvastatin is associated with a reduced incidence of dementia and Parkinson's disease.
Wolozin B1, Wang SW, Li NC, Lee A, Lee TA, Kazis LE.
Statins are a class of medications that reduce cholesterol by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Whether statins can benefit patients with dementia remains unclear because of conflicting results. We hypothesized that some of the confusion in the literature might arise from differences in efficacy of different statins. We used a large database to compare the action of several different statins to investigate whether some statins might be differentially associated with a reduction in the incidence of dementia and Parkinson's disease.
We analyzed data from the decision support system of the US Veterans Affairs database, which contains diagnostic, medication and demographic information on 4.5 million subjects. The association of lovastatin, simvastatin and atorvastatin with dementia was examined with Cox proportional hazard models for subjects taking statins compared with subjects taking cardiovascular medications other than statins, after adjusting for covariates associated with dementia or Parkinson's disease.
We observed that simvastatin is associated with a significant reduction in the incidence of dementia in subjects > or =65 years, using any of three models. The first model incorporated adjustment for age, the second model included adjusted for three known risk factors for dementia, hypertension, cardiovascular disease or diabetes, and the third model incorporated adjustment for the Charlson index, which is an index that provides a broad assessment of chronic disease. Data were obtained for over 700,000 subjects taking simvastatin and over 50,000 subjects taking atorvastatin who were aged >64 years. Using model 3, the hazard ratio for incident dementia for simvastatin and atorvastatin are 0.46 (CI 0.44-0.48, p < 0.0001) and 0.91 (CI 0.80-1.02, p = 0.11), respectively. Lovastatin was not associated with a reduction in the incidence of dementia. Simvastatin also exhibited a reduced hazard ratio for newly acquired Parkinson's disease (HR 0.51, CI 0.4-0.55, p < 0.0001).
Simvastatin is associated with a strong reduction in the incidence of dementia and Parkinson's disease, whereas atorvastatin is associated with a modest reduction in incident dementia and Parkinson's disease, which shows only a trend towards significance.
PMID: 17640385 [PubMed - indexed for MEDLINE] PMCID: PMC1955446