Potential Neuroregenerative and Neuroprotective Effects of Uridine/Choline-Enriched Multinutrient Dietary Intervention for Mild Cognitive Impairment: A Narrative Review.

In mild cognitive impairment (MCI) due to Alzheimer disease (AD), also known as prodromal AD, there is evidence for a pathologic shortage of uridine, choline, and docosahexaenoic acid [DHA]), which are key nutrients needed by the brain. Preclinical and clinical evidence shows the importance of nutrient bioavailability to support the development and maintenance of brain structure and function in MCI and AD. Availability of key nutrients is limited in MCI, creating a distinct nutritional need for uridine, choline, and DHA.

The Trajectory from Mood to Obesity.

Purpose Of Review: To describe and explain the relationships between mood disturbances and the development of obesity.

Recent Findings: That depression, anxiety, PTSD, or severe stresses can promote obesity as a side-effect of the drugs used to treat them, or through "carbohydrate craving" to enhance brain serotonin synthesis and alleviate dysphoria by consuming foods that are rich in both carbohydrates and fats. That seasonal affective disorder and severe PMS can independently cause patients to overconsume foods rich in both carbohydrates and fats.

Synapse formation in the brain can be enhanced by co-administering three specific nutrients.

The memory impairments of early Alzheimer's disease [AD] are thought to result from a deficiency in synapses within the hippocampus and related brain regions. This deficiency could result from an acceleration in synapse turnover - perhaps caused by an endogenous neurotoxin like A-beta oligomers - or from a decrease in the production of the synaptic membrane needed to form new synapses. An AD-associated decrease in synaptogenesis almost certainly does occur, inasmuch as major decreases are also observed in the numbers of hippocampal dendritic spines, the immediate cytologic precursor of glutamatergic synapses.