title: Souvenaid®: a new approach to management of early Alzheimer's disease.
abstract: Synaptic loss correlates closely with cognitive deficits in Alzheimer's disease and represents a new target for intervention. Souvenaid® is the first medical nutrition product to be designed to support synapse formation and function in early Alzheimer's disease, and has undergone an extensive, 12-year development programme. The relatively large amount of clinical data available for Souvenaid® is unusual for a medical nutrition product. Souvenaid® contains omega-3 polyunsaturated fatty acids (docosahexaenoic acid and eicosapentaenoic acid), uridine (as uridine monophosphate) and choline which are nutritional precursors required for synaptic membrane phospholipid synthesis, together with phospholipids and other cofactors. Souvenaid® has demonstrated cognitive benefits in patients with mild Alzheimer's disease but not in patients with mild-to-moderate Alzheimer's disease. Two randomised, double-blind, controlled trials (duration 12 and 24 weeks) in patients with mild Alzheimer's disease untreated with acetylcholinesterase inhibitors and/or memantine have demonstrated that Souvenaid® is well tolerated and improves episodic memory performance. The daily intake of Souvenaid® has not been associated with any harmful effects or interactions with medications and none are anticipated. The ongoing, 24-month, European Union-funded LipiDiDiet trial in subjects with prodromal Alzheimer's disease is evaluating the potential benefits of Souvenaid® on memory and in slowing progression to Alzheimer's dementia. If Souvenaid® induces synaptogenesis and improved synaptic function, it may provide benefits in other clinical conditions characterised by neurodegeneration. A number of trials are ongoing and planned to evaluate the potential wider benefits of Souvenaid®.
authors.affiliation: C Ritchie, Department of Medicine, Imperial College, London, UK, c.ritchie@imperial.ac.uk; npeaker@mednetconsult.co.uk.
authors.forename: C W
authors.initials: CW
authors.lastname: Ritchie
authors.forename: J
authors.initials: J
authors.lastname: Bajwa
authors.forename: G
authors.initials: G
authors.lastname: Coleman
authors.forename: K
authors.initials: K
authors.lastname: Hope
authors.forename: R W
authors.initials: RW
authors.lastname: Jones
authors.forename: M
authors.initials: M
authors.lastname: Lawton
authors.forename: M
authors.initials: M
authors.lastname: Marven
authors.forename: P
authors.initials: P
authors.lastname: Passmore
mesh_terms: D000544:Alzheimer Disease / Q000178:diet therapy* / Q000473:pathology / Q000503:physiopathology; D002794:Choline / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D002800:Cholinesterase Inhibitors; D018450:Disease Progression; D004281:Docosahexaenoic Acids / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D004311:Double-Blind Method; D015118:Eicosapentaenoic Acid / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D005062:European Union; D005260:Female; D006801:Humans; D008297:Male; D008559:Memantine; D061212:Memory, Episodic; D062706:Prodromal Symptoms; D016032:Randomized Controlled Trials as Topic; D013569:Synapses / Q000187:drug effects; D014542:Uridine Monophosphate / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D002800:Cholinesterase Inhibitors; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D014542:Uridine Monophosphate; D002794:Choline; D008559:Memantine