Parkinson's Disease Tulip


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Old 01-08-2010, 12:39 PM #1
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Default PD too? Why not?

http://www.dailymail.co.uk/health/ar...ts-memory.html
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 01-08-2010, 02:44 PM #2
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cool.....but why does it take so long to get things on the market?
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Old 01-08-2010, 05:00 PM #3
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Rick, I don't know if this could help us or not.

From the abstract:

Conclusions

Supplementation with a medical food including phosphatide precursors and cofactors for 12 weeks improved memory (delayed verbal recall) in mild AD patients. This proof-of-concept study justifies further clinical trials.

4. Discussion

In this randomized, double-blind, controlled multicenter trial we demonstrated that patients with mild AD who consumed the medical food Souvenaid for 12 weeks experienced a statistically significant improvement in WMS-r–delayed verbal recall score versus controls (P = .026). Furthermore, in a prespecified subgroup analysis of patients with very mild AD, an improvement in delayed as well as immediate verbal recall was observed at 12 weeks in those supplemented with active product versus controls. Excellent compliance (>95%) was confirmed by markedly increased DHA and EPA levels in erythrocyte membranes, elevated plasma vitamin E, and concomitant reduction in plasma homocysteine.

No differences were observed between active and control groups either in biochemical safety markers or in the incidence of adverse events or severe adverse events. With patients from 29 AD treatment centers from 5 countries, the results of this study are robust.

To our knowledge, this is the first multicenter, controlled clinical trial to show that a treatment designed to restore synapses through nutritional supplementation [3] can provide significant benefits to patients with mild AD. Although several preclinical studies have demonstrated the potential of various nutrients (single or in combination) to positively affect the pathophysiology and symptoms of AD, clinical evidence is scant.

Moreover, none of these earlier studies has chosen nutrients based on their ability, jointly, to promote synaptogenesis. Previous studies on nutrients and cognition have, in general, used epidemiological methods to assess potential relations between diet or specific nutrients and the risk of developing AD or dementia, or developed trials based on hypothesis derived from these epidemiological studies. A few small studies have reported the benefits of certain nutrients in people with confirmed dementia or AD, e.g., B vitamins [28], EPA [29], and omega-3 fatty acids [30].

Although the results of these studies suggest, at best, a moderate effect of single nutrients, the findings of our study demonstrate that a specific combination of nutrients with known neurochemical effects has the potential to provide clinically significant benefits to patients with AD. The observed effectiveness of the combined nutrients in our novel medical food, utilizing the body's normal metabolic pathways, is in line with synergistic actions demonstrated in preclinical studies [3], [4], [10] and [31].

The underlying hypothesis tested in the present study was based on observations that (1) cognitive decline in AD correlates with loss of synapses [1] and [2]; (2) patients with AD appear to be subclinically deficient in certain nutrients, some of which are required for synaptic membrane synthesis [32] E.M. van der Beek and P.J. Kamphuis, The potential role of nutritional components in the management of Alzheimer's disease, Eur J Pharmacol 585 (2008), pp. 197–207. Abstract | View Record in Scopus | Cited By in Scopus (2)[32]; and

(3) preclinical studies show that combined administration of specific nutrients increases brain levels of synaptic membrane [3] and enhances cognitive functions [10] and [11].

Uridine monophosphate, DHA, and choline act synergistically to increase brain phosphatides and synaptic protein levels, and those of hippocampal dendritic spines [6], at least 96% of which are thought to become new synapses by attaching to a terminal bouton of a presynaptic neuron [7].

The medical food used in this study provides phosphatide precursors, as well as B vitamins (for endogenous choline synthesis), vitamins C and E, selenium, and phospholipids, which further enhance membrane formation, integrity, and function.

The latest preclinical findings show that combined administration of this specific mixture of nutrients is more effective than single nutrients at improving membrane-bound cholinergic receptor functioning [33], and at reducing beta-amyloid production, plaque burden, and neurodegeneration in the APP/PS1 mouse model of AD pathology [31].

In terms of a human model to support biological plausibility, it has been proposed that patients with AD may have specific nutrient needs that could be a consequence of the disease process itself, or reflect a low intake or reduced bioavailability of specific nutrients needed for synapse synthesis and function [32].

An emerging nutritional deficiency may accelerate the disease process. Altogether, there is a compelling body of evidence in support of the proposition that administration of phosphatide precursors in combination with cofactors stimulates synapse formation and mitigates pathological processes in AD [32].......

In conclusion, this proof-of-concept study showed that supplementation with the multi-nutrient drink Souvenaid for 12 weeks is well-tolerated and results in an improvement in memory in patients with mild AD. Further clinical trials with this product in patients with AD are justified, with Souvenaid given both as add-on therapy in patients with mild to moderate AD receiving approved anti-AD medication, and in drug-naïve patients in order to confirm and extend the results of the current study.

Future clinical trials aim to measure relevant biomarkers, in support of the hypothesis that Souvenaid can improve synapse formation. Measurement of cerebrospinal fluid biomarkers to show brain penetration and exposure as well as brain imaging (magnetic resonance imaging) will be addressed in the LipiDiDiet Study (NTR5433), and electroencephalogram and magnetoencephalogram in the Souvenir II Study (NTR1975). These trials have started in Europe, as well as in the United States (S-Connect Study, NTR1683).

http://www.sciencedirect.com/science...47a680c7c29422
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