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Targeting synaptic dysfunction in Alzheimer's disease by administering a specific nutrient combination.
J Alzheimers Dis 2014; 38(3):459-79JA

Abstract

Synapse loss and synaptic dysfunction are pathological processes already involved in the early stages of Alzheimer's disease (AD). Synapses consist principally of neuronal membranes, and the neuronal and synaptic losses observed in AD have been linked to the degeneration and altered composition and structure of these membranes. Consequently, synapse loss and membrane-related pathology provide viable targets for intervention in AD. The specific nutrient combination Fortasyn Connect (FC) is designed to ameliorate synapse loss and synaptic dysfunction in AD by addressing distinct nutritional needs believed to be present in these patients. This nutrient combination comprises uridine, docosahexaenoic acid, eicosapentaenoic acid, choline, phospholipids, folic acid, vitamins B12, B6, C, and E, and selenium, and is present in Souvenaid, a medical food intended for use in early AD. It has been hypothesized that FC counteracts synaptic loss and reduces membrane-related pathology in AD by providing nutritional precursors and cofactors that act together to support neuronal membrane formation and function. Preclinical studies formed the basis of this hypothesis which is being validated in a broad clinical study program investigating the potential of this nutrient combination in AD. Memory dysfunction is one key early manifestation in AD and is associated with synapse loss. The clinical studies to date show that the FC-containing medical food improves memory function and preserves functional brain network organization in mild AD compared with controls, supporting the hypothesis that this intervention counteracts synaptic dysfunction. This review provides a comprehensive overview of basic scientific studies that led to the creation of FC and of its effects in various preclinical models.

Authors+Show Affiliations

Nutricia Advanced Medical Nutrition, Nutricia Research, Utrecht, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

23985420

Citation

van Wijk, Nick, et al. "Targeting Synaptic Dysfunction in Alzheimer's Disease By Administering a Specific Nutrient Combination." Journal of Alzheimer's Disease : JAD, vol. 38, no. 3, 2014, pp. 459-79.
van Wijk N, Broersen LM, de Wilde MC, et al. Targeting synaptic dysfunction in Alzheimer's disease by administering a specific nutrient combination. J Alzheimers Dis. 2014;38(3):459-79.
van Wijk, N., Broersen, L. M., de Wilde, M. C., Hageman, R. J., Groenendijk, M., Sijben, J. W., & Kamphuis, P. J. (2014). Targeting synaptic dysfunction in Alzheimer's disease by administering a specific nutrient combination. Journal of Alzheimer's Disease : JAD, 38(3), pp. 459-79. doi:10.3233/JAD-130998.
van Wijk N, et al. Targeting Synaptic Dysfunction in Alzheimer's Disease By Administering a Specific Nutrient Combination. J Alzheimers Dis. 2014;38(3):459-79. PubMed PMID: 23985420.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting synaptic dysfunction in Alzheimer's disease by administering a specific nutrient combination. AU - van Wijk,Nick, AU - Broersen,Laus M, AU - de Wilde,Martijn C, AU - Hageman,Robert J J, AU - Groenendijk,Martine, AU - Sijben,John W C, AU - Kamphuis,Patrick J G H, PY - 2013/8/30/entrez PY - 2013/8/30/pubmed PY - 2014/7/18/medline KW - Alzheimer's disease KW - Fortasyn Connect KW - Souvenaid KW - amyloid-β KW - membrane KW - neurotransmission KW - nutrition KW - phospholipid KW - synaptic dysfunction SP - 459 EP - 79 JF - Journal of Alzheimer's disease : JAD JO - J. Alzheimers Dis. VL - 38 IS - 3 N2 - Synapse loss and synaptic dysfunction are pathological processes already involved in the early stages of Alzheimer's disease (AD). Synapses consist principally of neuronal membranes, and the neuronal and synaptic losses observed in AD have been linked to the degeneration and altered composition and structure of these membranes. Consequently, synapse loss and membrane-related pathology provide viable targets for intervention in AD. The specific nutrient combination Fortasyn Connect (FC) is designed to ameliorate synapse loss and synaptic dysfunction in AD by addressing distinct nutritional needs believed to be present in these patients. This nutrient combination comprises uridine, docosahexaenoic acid, eicosapentaenoic acid, choline, phospholipids, folic acid, vitamins B12, B6, C, and E, and selenium, and is present in Souvenaid, a medical food intended for use in early AD. It has been hypothesized that FC counteracts synaptic loss and reduces membrane-related pathology in AD by providing nutritional precursors and cofactors that act together to support neuronal membrane formation and function. Preclinical studies formed the basis of this hypothesis which is being validated in a broad clinical study program investigating the potential of this nutrient combination in AD. Memory dysfunction is one key early manifestation in AD and is associated with synapse loss. The clinical studies to date show that the FC-containing medical food improves memory function and preserves functional brain network organization in mild AD compared with controls, supporting the hypothesis that this intervention counteracts synaptic dysfunction. This review provides a comprehensive overview of basic scientific studies that led to the creation of FC and of its effects in various preclinical models. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/23985420/Targeting_synaptic_dysfunction_in_Alzheimer's_disease_by_administering_a_specific_nutrient_combination_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-130998 DB - PRIME DP - Unbound Medicine ER -