Abstract
Brain neurons form synapses throughout the life span. This process is initiated by neuronal depolarization, however the numbers of synapses thus formed depend on brain levels of three key nutrients—uridine, the omega-3 fatty acid DHA, and choline. Given together, these nutrients accelerate formation of synaptic membrane, the major component of synapses. In infants, when synaptogenesis is maximal, relatively large amounts of all three nutrients are provided in bioavailable forms (e.g., uridine in the UMP of mothers’ milk and infant formulas). However, in adults the uridine in foods, mostly present at RNA, is not bioavailable, and no food has ever been compelling demonstrated to elevate plasma uridine levels. Moreover, the quantities of DHA and choline in regular foods can be insufficient for raising their blood levels enough to promote optimal synaptogenesis. In Alzheimer’s disease (AD) the need for extra quantities of the three nutrients is enhanced, both because their basal plasma levels may be subnormal (reflecting impaired hepatic synthesis), and because especially high brain levels are needed for correcting the disease-related deficiencies in synaptic membrane and synapses.
Highlights
The recognition that nutrient intake can affect the rate at which the brain makes new synapses arose largely from basic-science studies performed in MIT’s Department of Brain and CognitiveSciences between 1999 and 2012 [1,2,3,4]
These studies showed that when three nutrients—uridine; the omega-3 fatty acid docosahexaenoic acid (DHA); and choline—are consumed together, brain cells produce more of the specialized membranes [1] used for forming dendritic spines [2,3], the immediate anatomic precursor of synapses
The ability of the brain to make more phosphatidylcholine (PC), and related membrane constituents when presented with additional uridine, DHA, and choline, requires that the enzymes which catalyze the steps in PC synthesis have a special biochemical property: Each enzyme must exhibit unusually poor affinity for its substrate, so that, at the uridine, DHA, and choline concentrations normally present in brain cells, many enzyme molecules will not be attached to their substrate and, will not be able to act on it
Summary
Sciences between 1999 and 2012 [1,2,3,4] As described below, these studies showed that when three nutrients—uridine (as its monophosphate, UMP); the omega-3 fatty acid DHA (or EPA, which is Nutrients 2014, 6 effective [4]); and choline—are consumed together, brain cells produce more of the specialized membranes [1] used for forming dendritic spines [2,3], the immediate anatomic precursor of synapses. An additional biochemical mechanism activated by the uridine in SOUVENAID® enables the brain to increase production of the special proteins found in synaptic membranes. It involves the activation of P2Y receptors, a particular family of brain receptors that can affect neuronal differentiation and synaptic protein synthesis [10]. P2Y receptor activation is involved in the processes that shape the newly-formed membrane into neurites, dendritic spines, and synapse [10]
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