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Choline as a prevention for Alzheimer’s disease
Author(s) -
Ramón Velázquez,
Wendy Winslow,
Marc A. Mifflin
Publication year - 2020
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.102849
Subject(s) - alzheimer's disease , disease , choline , neuroscience , medicine , psychology , pathology
the U.S. and is projected to afflict 14 million Americans by 2050 [1]. The costs associated with managing AD are expected to exceed $20 trillion in the same time span [1]. The neuropathologies in AD include, Amyloid-β (Aβ) plaques, neurofibrillary tangles, and neuronal loss, which are associated with cognitive impairments [1]. Notably, microglia, the brains resident immune cells, are specialized to rid the brain of deleterious debris. Although microglia keep the brain healthy, if they are overactivated, brain inflammation and neuronal death occurs [2]. To date, no treatments have been developed to effectively slow the progression of AD. A multitude of factors are believed to contribute to the development of the disease, including genetics (e.g. APOE status), age and lifestyle [2]. Interestingly, for reasons that remain unknown, females have an increased risk of developing AD [1). Moreover, studies have identified diet as a significant factor associated with preventing cognitive decline [2]. Collectively, this was the basis of our recent publication that examined the role of lifelong dietary choline supplementation in the APP/PS1 AD mouse model (Figure 1) [3]. Choline is a B-like nutrient that is endogenously produced by the human body. However, endogenous production fails to meet bodily demands. Dietary choline can be found in common foods. In 1998, the U.S. established a recommended daily intake (RDI) of dietary choline for adult women (425mg/day) and adult men (550mg/day). Choline is required to produce acetylcholine, a neurotransmitter responsible for memory, muscle control and mood. It also builds cell membranes and plays a vital role in regulating gene expression. A converging line of evidence indicates that the current RDI may not be optimal for proper brain health and cognition [2–4]. Decades of research have shown that supplementing the maternal (gestation and lactation) diet with choline produces profound benefits on the offspring’s brain health and cognition [5,6]. In fact, studies have demonstrated amelioration of cognitive deficits in mouse models of Down syndrome and AD [5,6]. Remarkably, a very recent study found that maternal choline supplementation (MCS) can produce transgenerational benefits on AD neuropathology, which has profound implications for generations to come [6]. Editorial

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