Abstract
Enhancing Synaptogenesis in Diseases Characterized by Deficiencies in Brain Synapses
Highlights
In the future perhaps another drug candidate might succeed both in reducing brain levels of A-beta peptides and ameliorating the dementia of Alzheimer’s Disease; mankind appears united in the hope that this will be the case
There are a number of loci at which such a treatment might work: For example, it might amplify the flux of free calcium into stimulated dendrites, or activate receptors that control key steps in forming dendritic spines, or increase the synthesis of pre- or post-synaptic proteins, or generate more synaptic membrane, the main constituent of synapses
Because the enzymes that initiate the conversion of these compounds to PC are unsaturated, the administration of choline increases the synthesis and brain levels of its phosphorylated product phosphocholine; that of uridine increases UTP and CTP; and that of docosahexaenoic acid (DHA) increases the proportion of diacylglycerol (DAG) that contains this omega-3 fatty acid
Summary
In the future perhaps another drug candidate might succeed both in reducing brain levels of A-beta peptides and ameliorating the dementia of Alzheimer’s Disease; mankind appears united in the hope that this will be the case. There are a number of loci at which such a treatment might work: For example, it might amplify the flux of free calcium into stimulated dendrites, or activate receptors that control key steps in forming dendritic spines, or increase the synthesis of pre- or post-synaptic proteins, or generate more synaptic membrane, the main constituent of synapses.
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