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Oral administration of circulating precursors for membrane phosphatides can promote the synthesis of new brain synapses
Author(s) -
Cansev Mehmet,
Wurtman Richard J.,
Sakamoto Toshimasa,
Ulus Ismail H.
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2007.10.005
Subject(s) - neurotransmission , docosahexaenoic acid , postsynaptic potential , neurotransmitter , arachidonic acid , neurochemical , neuroscience , neurotransmitter receptor , monoamine neurotransmitter , eicosapentaenoic acid , synaptic cleft , chemistry , biochemistry , biology , fatty acid , medicine , receptor , polyunsaturated fatty acid , serotonin , enzyme
Although cognitive performance in humans and experimental animals can be improved by administering omega‐3 fatty acid docosahexaenoic acid (DHA), the neurochemical mechanisms underlying this effect remain uncertain. In general, nutrients or drugs that modify brain function or behavior do so by affecting synaptic transmission, usually by changing the quantities of particular neurotransmitters present within synaptic clefts or by acting directly on neurotransmitter receptors or signal‐transduction molecules. We find that DHA also affects synaptic transmission in mammalian brain. Brain cells of gerbils or rats receiving this fatty acid manifest increased levels of phosphatides and of specific presynaptic or postsynaptic proteins. They also exhibit increased numbers of dendritic spines on postsynaptic neurons. These actions are markedly enhanced in animals that have also received the other two circulating precursors for phosphatidylcholine, uridine (which gives rise to brain uridine diphosphate and cytidine triphosphate) and choline (which gives rise to phosphocholine). The actions of DHA aere reproduced by eicosapentaenoic acid, another omega‐3 compound, but not by omega‐6 fatty acid arachidonic acid. Administration of circulating phosphatide precursors can also increase neurotransmitter release (acetylcholine, dopamine) and affect animal behavior. Conceivably, this treatment might have use in patients with the synaptic loss that characterizes Alzheimer's disease or other neurodegenerative diseases or occurs after stroke or brain injury.