Souvenaid

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Souvenaid is a medical nutrition formulation, presented as a drink, that has been studied for potential use in the dietary management of early Alzheimer's disease.[1] A NPS MedicineWise summary stated (based on three randomized controlled trials) that Souvenaid failed to show a significant effect in decreasing the rate of cognitive decline or delaying progression of Alzheimer's disease, but that there may be a minor improvement in memory in drug naive people in the very early stages of the disease.[2]

Souvenaid was developed by Advanced Medical Nutrition division of Nutricia and contains a patented combination of nutrients, referred to under the trademark Fortasyn Connect.[3]

Composition[edit]

The composition of Souvenaid includes:[4]

Development of concept[edit]

Souvenaid is the result of research by investigators from the Massachusetts Institute of Technology (MIT), and other international groups being conducted since 2002. Much of the research was led by MIT Professor Richard Wurtman.[5] Souvenaid was designed to support synapse formation and function[1] in early Alzheimer's disease.

The concept of Souvenaid is based on the fact that loss of synapses is one of the hallmarks of Alzheimer's disease and that this hallmark correlates best with memory impairment.[6][7][8] There is evidence in the scientific literature that individuals with this condition may lack adequate levels of nutrients important for the formation of new synapses in order to compensate for the experienced loss.[9][10][11][12][13][14][15] Souvenaid has been studied in pre-clinical and clinical studies.

References[edit]

  1. ^ a b Sijben JWC, de Wilde MC, Wieggers R, Groenendijk M, Kamphuis PJGH. A multi nutrient concept to enhance synapse formation and function: science behind a medical food for Alzheimer's disease. OCL 2011;18:267-270. doi : 10.1684/ocl.2011.0410
  2. ^ "Souvenaid: help for people with Alzheimer’s disease?". NPS MedicineWise. Published in Health News and Evidence. 2014-01-15. 
  3. ^ "Souvenaid Consumer : Home". souvenaid.nutricia.com. Retrieved 2014-04-22. 
  4. ^ "Medscape: Medscape Access". medscape.com. Retrieved 2014-04-22. 
  5. ^ Scheltens P, Kamphuis PJ, Verhey FR, et al. (January 2010). "Efficacy of a medical food in mild Alzheimer's disease: A randomized, controlled trial". Alzheimers Dement. 6 (1): 1–10.e1. PMID 20129316. doi:10.1016/j.jalz.2009.10.003. 
  6. ^ Terry RD, Masliah E, Salmon DP, et al. (October 1991). "Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment". Ann. Neurol. 30 (4): 572–80. PMID 1789684. doi:10.1002/ana.410300410. 
  7. ^ Terry RD (September 2006). "Alzheimer's disease and the aging brain". J Geriatr Psychiatry Neurol. 19 (3): 125–8. PMID 16880353. doi:10.1177/0891988706291079. 
  8. ^ Sperling RA, Aisen PS, Beckett LA, et al. (May 2011). "Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease". Alzheimers Dement. 7 (3): 280–92. PMC 3220946Freely accessible. PMID 21514248. doi:10.1016/j.jalz.2011.03.003. 
  9. ^ Glasø M, Nordbø G, Diep L, Bøhmer T (2004). "Reduced concentrations of several vitamins in normal weight patients with late-onset dementia of the Alzheimer type without vascular disease". J Nutr Health Aging. 8 (5): 407–13. PMID 15359361. 
  10. ^ Köseoglu E, Karaman Y (August 2007). "Relations between homocysteine, folate and vitamin B12 in vascular dementia and in Alzheimer disease". Clin. Biochem. 40 (12): 859–63. PMID 17532313. doi:10.1016/j.clinbiochem.2007.04.007. 
  11. ^ Polidori MC, Mattioli P, Aldred S, et al. (2004). "Plasma antioxidant status, immunoglobulin g oxidation and lipid peroxidation in demented patients: relevance to Alzheimer disease and vascular dementia". Dement Geriatr Cogn Disord. 18 (3-4): 265–70. PMID 15286458. doi:10.1159/000080027. 
  12. ^ Conquer JA, Tierney MC, Zecevic J, Bettger WJ, Fisher RH (December 2000). "Fatty acid analysis of blood plasma of patients with Alzheimer's disease, other types of dementia, and cognitive impairment". Lipids. 35 (12): 1305–12. PMID 11201991. doi:10.1007/s11745-000-0646-3. 
  13. ^ Ravaglia G, Forti P, Maioli F, et al. (August 2004). "Plasma amino acid concentrations in patients with amnestic mild cognitive impairment or Alzheimer disease". Am. J. Clin. Nutr. 80 (2): 483–8. PMID 15277174. 
  14. ^ Corrigan FM, Van Rhijn AG, Ijomah G, et al. (August 1991). "Tin and fatty acids in dementia". Prostaglandins Leukot. Essent. Fatty Acids. 43 (4): 229–38. PMID 1946550. doi:10.1016/0952-3278(91)90035-4. 
  15. ^ Corrigan FM, Horrobin DF, Skinner ER, Besson JA, Cooper MB (February 1998). "Abnormal content of n-6 and n-3 long-chain unsaturated fatty acids in the phosphoglycerides and cholesterol esters of parahippocampal cortex from Alzheimer's disease patients and its relationship to acetyl CoA content". Int. J. Biochem. Cell Biol. 30 (2): 197–207. PMID 9608673. doi:10.1016/s1357-2725(97)00125-8.