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From Scientific American:
http://www.scientificamerican.com/blog/ ... 2010-07-12

Low vitamin D in Parkinsons and Dementia--

"The first study, led by Paul Knekt and colleagues at the National Institute for Health and Welfare, Finland, examined levels of vitamin D in the blood of 3,173 Finnish men and women aged 50-79 determined to be free of Parkinson's disease at the start of the study. The researchers then examined the incidence of Parkinson's disease in these participants over a 29-year follow-up period. They found that participants with the highest levels of vitamin D (more than 50 nmol/L) had a 65 percent lower risk of developing Parkinson's disease than those with the lowest vitamin D levels (less than 25 nmol/L).

In the second study, David Llewellyn of the University of Exeter and colleagues examined vitamin D levels among 858 Italian men and women age 65 and older. They found that more than half of the participants with dementia were vitamin D deficient .
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And here is news of a study at SUNY Buffalo, from earlier this spring:

"Low vitamin D levels may be associated with more advanced physical disability and cognitive impairment in persons with multiple sclerosis, studies conducted by neurologists at the University at Buffalo have shown.
http://www.sciencedaily.com/releases/20 ... 153955.htm

Their results, reported at the American Academy of Neurology meeting, held earlier this month, indicated that:
The majority of MS patients and healthy controls had insufficient vitamin D levels.
Clinical evaluation and magnetic resonance imaging (MRI) images show low blood levels of total vitamin D and certain active vitamin D byproducts are associated with increased disability, brain atrophy and brain lesion load in MS patients.

A potential association exists between cognitive impairment in MS patients and low vitamin D levels."

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Now, how could this situation be compounded when we consider CCSVI as a factor in developing MS? I believe it's all about protecting the brain from further vascular damage. Here's a wonderful research paper on how Vitamin D can provide "vasculoprotection" of the brain.

http://ddr.nal.usda.gov/bitstream/10113 ... 182071.pdf

"Vitamin D may help to protect against cognitive deterioration and dementia, specifically, vascular dementia and Alzheimer’s disease, through vasculoprotection (Lind et al., 1987; Burgess et al., 1990; O’Connell et al., 1997; Pfeifer et al., 2001; Wang et al., 2001; Zittermann et al., 2003; Wang et al., 2008a,b), preservation of neurons (Sutherland et al., 1992; Landfield and Cadwallader-Neal, 1998; Brewer et al., 2001), and protection against risk factors for cognitive dysfunction (Lind et al., 1987; Burgess et al., 1990; Hypponen et al., 2001; Pfeifer et al., 2001; Li et al., 2002, 2004; Zittermann et al., 2003; Bisc- hoff-Ferrari et al., 2004; Wang et al., 2008a,b).

We did observe an inverse association between 25(OH) D concentration and presence of white matter hyperintensities and large vessel infarcts; indicators of cerebrovascular disease (Buell et al, in preparation). Consistent with this finding, we observed a positive association between vitamin D concentrations and the integrity and structural arrangement of white matter fibers using diffuser tensor imaging. Further studies designed to provide information on the temporal relationship of 25(OH)D and brain morphology are warranted.
420 J.S. Buell, B. Dawson-Hughes / Molecular Aspects of Medicine 29 (2008) 415–422"

Researchers, lead by a team from Oxford, have been looking for genetic clues to explain the potential cause of MS. Their investigations identified a mutation of a gene, CYP27B1. They then looked at 3,000 families of unaffected parents with a child with MS and found that 35 parents carried this variant gene and had passed it on to their child.

This gene variant is rare and does not account for all cases of MS. But what is interesting is that this gene variant can cause vitamin D deficiency. The results of this study strengthen the case for vitamin D deficiency as one of the potential causes of MS.

se1956 wrote:and/or
liver metabolism defect (my guess)

Because a woman went from EDSS 5 to zero in 3 years after a liver transplant.

While there were no differences between the groups in MRI findings, clinical status worsened in the high-dose group, with a median disability score of 3 at six months compared with a median score of 2 in the low-dose group (P=0.04). The final disability score correlated with the baseline score (r = 0.79, P<0.001). Among the 11 patients receiving the high dose, four had clinical relapses during the study, compared with none in the low-dose group (P=0.04). A possible explanation for the differences between the groups on clinical outcomes, though not on MRI results, could reflect changes in response to their glatiramer or interferon, though this would need to be explored in larger trials, according to the investigators.

"Correlations of lower MS prevalence, activity, and mortality with high levels of vitamin D3 nutrition have led to the hypothesis that high levels of vitamin D could be beneficial for MS," they observed.

"Our [randomized clinical trial] outcomes do not support this hypothesis," they stated.

NHE wrote:Interesting. Do you have a link for this news regarding the liver transplant? That would be great to read.

se1956 wrote:Because a woman went from EDSS 5 to zero in 3 years after a liver transplant.

R.

Liver transplantation as a cure for acute intermittent porphyria
Original Text
Zahir F Soonawalla MS a, Taner Orug MD a, Michael N Badminton MRCPath b, Prof George H Elder MD b, Prof Jonathan M Rhodes MD c, Simon R Bramhall MD a, Elwyn Elias MD a Summary
Acute intermittent porphyria occasionally causes frequent and crippling acute neurovisceral attacks associated with increased hepatic production of porphyrin precursors, resulting in long-term damage, poor quality of life, and shortened life expectancy. There has been no cure for this condition, but replacement of deficient hepatic enzymes might restore excretion of porphyrin precursors to normal and prevent acute attacks. We aimed to treat severe acute intermittent porphyria in a 19-year-old woman by liver transplantation. After the transplant, concentrations of haem precursors in the patient's urine returned to normal, and 1·5 years later her quality of life was good. Our report suggests some hope of cure for selected patients with severe forms of this disease

Also known asVDR; CP2B; CYP1; PDDR; VDD1; VDDR; VDDRI; CYP27B; P450c1; CYP1alpha
Summary: This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. The protein encoded by this gene localizes to the inner mitochondrial membrane where it hydroxylates 25-hydroxyvitamin D3 at the 1alpha position. This reaction synthesizes 1alpha,25-dihydroxyvitamin D3, the active form of vitamin D3, which binds to the vitamin D receptor and regulates calcium metabolism. Thus this enzyme regulates the level of biologically active vitamin D and plays an important role in calcium homeostasis. Mutations in this gene can result in vitamin D-dependent rickets type I. [provided by RefSeq, Jul 2008]

Cece wrote:Patients would not get a liver transplant without the immunosuppressive drugs so no way to separate out which one had the effect.