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Nutritional requirements in Alzheimer’s disease

Patients with early Alzheimer's disease have specific nutritional requirements to support synapse function and formation [1].

Nutrition plays a key role in the normal functioning and maintenance of the brain

The brain needs specific nutrients to build and maintain its structure [2].

It has been proven that adequate availability of vitamins, minerals, amino acids and fatty acids in the brain is critical for many neural functions. Additionally, nutritional deficiencies result in abnormal functions of the nervous system and clinical symptoms, including impaired cognition [2-4]

Lower nutrient status in patients with early Alzheimer’s disease

Systematic reviews and meta-analyses indicate consistently low levels of key nutrients in patients with early Alzheimer’s disease vs. age matched controls, even in the absence of malnutrition. Compromised nutritional status has been observed for nutrients such as omega-3 fatty acids (DHA, EPA), uridine, choline, B-vitamins, vitamin E, C and selenium [5-9].

Several factors are affecting the nutrient status of early Alzheimer’s disease patients [1]:  

  • Altered diet and nutrient intake
  • Reduced endogenous biosynthesis
  • Impaired nutrient uptake and absorption

Increased nutrient needs to counter synapse loss

Accelerated loss of synapses is a hallmark feature of memory loss in early Alzheimer’s disease [10]. This progressive loss leads to an increased need for key nutrients to build more neuronal membranes.  Indeed, synapse formation is dependent on rate-limiting nutritional precursors (omega-3 fatty acids, uridine, choline, phospholipids) and cofactors (vitamins B, vitamin E, C and selenium) [11].

Specific nutritional needs are difficult to address with a normal diet

It is therefore necessary to significantly increase the level of key nutrients to address the effect of accelerated synapse loss in patients with early Alzheimer’s disease [1]. It would be really difficult to modify the diet to achieve the right combination of the above mentioned specific nutrients and to expect patients to eat enough of the right foods daily. 

Souvenaid is designed to meet the specific nutritional needs of patients with early AD in order to support synapse formation

Souvenaid contains levels of nutrients that would be very difficult to achieve through a normal diet. The unique combination of nutrients is designed to meet the specific nutritional needs of early AD patients acting in synergy to support synapse formation [12]:

* Rate-limiting precursors: omega-3 fatty acids (EPA and DHA), uridine, choline, phospholipids

* Cofactors: B-vitamins, vitamin E, C and selenium.

In Souvenaid clinical trials, improvement in nutritional status is associated with improvement in memory in early Alzheimer’s disease patients [13-14]

  • Patients with early Alzheimer’s disease have a lower key nutrients status compared with age matched controls

    Patients with early Alzheimer’s disease have a lower key nutrients status compared with age matched controls

    Systematic review and meta-analyses demonstrates lower levels of Uridine, DHA, EPA, vitamin B12, folate, vitamin C and E, and Selenium in patients with early Alzheimer’s disease vs. age matched controls [5-9].

  • Hypothetical model of increased nutrient needs in patients with early Alzheimer‘s disease

    Hypothetical model of increased nutrient needs in patients with early Alzheimer‘s disease

    Patients with early Alzheimer's disease have specific nutritional requirements due to lower blood levels of the key nutrients for neuronal membranes and synapses and anincreased need to make new synapses to compensate for the loss in AD.
    These specific nutritional needs are not easily met by diet alone [1].

  • The level of key nutrients should be increased in order to counter synapse loss

    The level of key nutrients should be increased in order to counter synapse loss

    To counter synapse loss, it is necessary to not only return the levels of key nutrients back to normal, but to increase beyond [1]. This can be difficult to achieve through a normal diet.

  • Synapse loss correlates best with impaired memory

    Synapse loss correlates best with impaired memory

    Memory performance declines as the number of synapses decreases [10]. A specific combination of nutrients is required to support synapse formation [11-12].

  • Souvenaid is designed to meet the specific nutritional needs of patients with early AD to support synapse formation

    Souvenaid is designed to meet the specific nutritional needs of patients with early AD to support synapse formation

    Souvenaid has been clinically proven to improve memory in early Alzheimer’s disease patients [13,14].

References

  1. Kamphuis PJ and Scheltens P. Can nutrients prevent or delay onset of Alzheimer's disease? J Alzheimers Dis. 2010;20:765-775.
  2. Igarashi M, et al. Disturbed choline plasmalogen and phospholipid fatty acid concentrations in Alzheimer's disease prefrontal cortex. J Alzheimers Dis. 2011;24:507-517.
  3. Pettegrew JW, et al. Brain membrane phospholipid alterations in Alzheimer's disease. Neurochem Res. 2001;26:771-782.
  4. Mulder C, et al. Decreased lysophosphatidylcholine/phosphatidylcholine ratio in cerebrospinal fluid in Alzheimer's disease. J Neural Transm. 2003;110:949-955.
  5. Lopes Da Silva S, et al. Plasma nutrient status of Alzheimer’s disease patients compared to cognitive intact elderly controls: A systematic review and meta-analysis.  European Geriatric Medicine. 2012;3:85.
  6. Corrigan FM, et al. 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. 1998;30:197-207.
  7. Glasø M, et al. Reduced concentrations of several vitamins in normal weight patients with late-onset dementia of the Alzheimer type without vascular disease. J Nutr Health Aging 2004;8:407-413.
  8. Köseoglu E and Karaman Y. Relations between homocysteine, folate and vitamin B12 in vascular dementia and in Alzheimer disease. Clin Biochem. 2007;40:859-863.
  9. Polidori MC, et al. Plasma antioxidant status, immunoglobulin g oxidation and lipid peroxidation in demented patients: relevance to Alzheimer disease and vascular dementia. Dement Geriatr Cogn Disord. 2004;18:265-270.
  10. Conquer JA, et al. Fatty acid analysis of blood plasma of patients with Alzheimer's disease, other types of dementia, and cognitive impairment. Lipids. 2000;35:1305-1312.
  11. Ravaglia G, et al. Plasma amino acid concentrations in patients with amnestic mild cognitive impairment or Alzheimer disease. Am J Clin Nutr.2004;80:483-488.
  12. Corrigan FM, et al.Tin and fatty acids in dementia. Prostaglandins Leukot Essent Fatty Acids. 1991;43:229-238.
  13. Astarita G, et al. Deficient liver biosynthesis of docosahexaenoic acid correlates with cognitive impairment in Alzheimer's disease. PLoS One. 2010;5:e12538.
  14. Goodenowe DB, et al.Peripheral ethanolamine plasmalogen deficiency: a logical causative factor in Alzheimer's disease and dementia. J Lipid Res. 2007;48:2485-498.
  15. Van Dam F and Van Gool WA. Hyperhomocysteinemia and Alzheimer's disease: A systematic review. Arch Gerontol Geriatr. 2009;48:425-430.