This Is MS Multiple Sclerosis Community: Knowledge & Support

Really, I'm happy reading these results. But..

5 years ago, I started using 80 statine because of a similar trial. More research was nessasary, it ended...

And now, 5 years later.. same test, similar result, small group, so.... more resears is nessasary...



When are the results good enough? Why wait using statines. I don't!

_________________
I'm ready, I'm ready !

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 O, Waiczies S, Zipp F.
SourceInstitute 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

Here is the full text that will tell you what the novel therapeutic targets are.
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http://home.ix.netcom.com/~jdalton/egcg-neorond-ms.pdf

jackD

The results that are not good enough are "these drugs are so broadly used throughout the United States and the world, and to learn whether a relatively inexpensive oral therapy".

I have always read the word "inexpensive" to mean no money to be made, and therefore no funding for a trial.
Although, it does make me wonder why no one has looked to duplicate and create a substance that works on the same pathway as say Lipitor, but better; and therefore have a new patentable substance. Or is Lipitor (or whatever statn works for you, I originally tried Simvastatin) as good as it can be? or the modification to small to generate a new patent?

I too have been on 80mg Lipitor for a number of years, and it has been my main "DMD" medication (in my mind).

The link above appears to reference statins on the bottom of page 19. It also speaks about other things, not specifically Statins.

Thta other thing they talk about is EGCG (GREEN/WHITE TEA) Flavonoids and the fact that there seems to be a synergy between them.

I MUST state AGAIN AGAIN AGAIN that ZOCOR seems to be VERY superior to the other statins in protecting neurons.

jackD

p.s/. 80 mg of Lipitor is deadly and only 80 mg of Zocor is worse!!!

p.p.s. ONLY Zocor seems to get through the Blood Brain Barrier. Of course there is a possiblility that the MMP-9s may have made holes big enough is some MS folks for the other Statins to enter the brain.

http://home.ix.netcom.com/~jdalton/Yongrev.pdf

J Alzheimers Dis. 2011;23(2):307-18.

Statins as neuroprotectants: a comparative in vitro study of lipophilicity, blood-brain-barrier penetration, lowering of brain cholesterol, and decrease of neuron cell death.Sierra S, Ramos MC, Molina P, Esteo C, Vázquez JA, Burgos JS.

SourceBioPharma Division, Neuron BPh, Parque Tecnológico de Ciencias de la Salud, Edificio BIC, Armilla, Granada, Spain.

Abstract
There is growing evidence to support the hypothesis that statins may act as neuroprotectants in several neuropathological conditions, including Alzheimer's disease. The mechanisms for neuroprotection are only partially understood, however, and pleiotropic phenomena could be involved.

We have made a comparative study of 9 statins (lovastatin, mevastatin, pravastatin, simvastatin, cerivastatin, atorvastatin, fluvastatin, pitavastatin, and rosuvastatin), analyzing several parameters that could be related to neuroprotection, such as chemical structure, lipophilicity, potential blood-brain-barrier penetration (BBB), 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibition, cholesterol modulation in neurons, glia, and human hepatocyte cell lines, and protection against neurodegeneration caused by tau hyperphosphorylation induced by okadaic acid.

Our results indicate that monacolin J derivatives (natural and semi-synthetic statins) are the best candidates for the prevention of neurodegenerative conditions due to their higher potential BBB penetration capacity, cholesterol lowering effect on neurons with a satisfactory safety profile, and in vitro protection against cell death caused by okadaic acid in culture.

Among the nine statins studied, simvastatin presented the best characteristics for preventing neurodegenerative conditions.

PMID:21098985
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BMC Med. 2007 Jul 19;5:20.
Simvastatin is associated with a reduced incidence of dementia and Parkinson's disease.

Wolozin B, Wang SW, Li NC, Lee A, Lee TA, Kazis LE.
SourceBoston University School of Medicine, Boston, MA, USA. bwolozin@bu.edu

Abstract
BACKGROUND: 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.

METHODS:

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.

RESULTS: 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).

CONCLUSION: 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]

I first started with Simvastatin for about 6 months, many years ago. There were then a few studies that found Lipitor to be better, So I thought I would try switching. At the time, Simvastatin was appearing to be beneficial, so I was really scared of switching to Lipitor. However, a few hours after the first dose, I personally noticed a slight improvement in tingling in my feet. And other small improvements in the following weeks. At this stage, it is a personal choice by personal experience of what worked better for ME.

As for the "toxicity" of Lipitor, one of the other side benefits of Lipitor, is that it is not as sensitive to the time of day it has to be taken, as opposed to the others which are best taken at night (at least for cholesterol control). Because of this, I actually take the 80mg as two smaller divided doses of 40mg, thereby I hope to have a lower peak serum level at any one time. On my regular blood tests, my liver numbers are all within normal ranges and the indicator for muscle damage are also OK. So, so far so good.

Regarding its ability to cross the BBB, the original papers I read regarding statins lead me to believe that researches thought that their mode of action was actually in their ability to modulate (ie decrease) the permeability of the BBB, so actually measuring the content of spinal fluid for statins would not necessarily align to their effectiveness. Thanks for your concern.