Synaptic plasma membrane-bound acetylcholinesterase activity is not affected by docosahexaenoic acid-induced decrease in membrane order

Hossain, Shahdat; Hashimoto, Michio; Shimada, Toshio; Shido, Osamu

doi:10.1016/j.lfs.2003.10.028

Cited by 23 publications

(18 citation statements)

References 58 publications

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“…VCP senses and pulls abnormal protein accumulation in the cell, and pulls from the endoplasmic reticulum and nucleus [38]. DHAinduced clearance of Aβ from neuronal membranes is suggested to be mediated by exocytosis -a process that may be facilitated by the DHA-induced increase in membrane fluidity [24,39,40]. Consistently, EPA-induced memory augmentation is attributed to neurotransmitter (noradrenaline) release [10], as facilitated by an increase in membrane disorder (fluidity) [41].…”

Section: Discussionmentioning

confidence: 94%

The protective effect of dietary eicosapentaenoic acid against impairment of spatial cognition learning ability in rats infused with amyloid β(1–40)

Hashimoto

Hossain

Tanabe

et al. 2009

The Journal of Nutritional Biochemistry

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Section: Discussionmentioning

confidence: 94%

The protective effect of dietary eicosapentaenoic acid against impairment of spatial cognition learning ability in rats infused with amyloid β(1–40)

Hashimoto

Hossain

Tanabe

et al. 2009

The Journal of Nutritional Biochemistry

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“…When adult male rats were given DHA for 12 weeks, the DHA content of cell membranes was increased with a concomitant increase in the fluidity of the membrane, but AChE activity in the cortex was unchanged by DHA supplementation [34]. These differences in the effects of PUFAs on AChE activity may be due to the extent of incorporation of specific PUFAs into the cell membrane.…”

Section: Ache Inhibitionmentioning

confidence: 96%

Dietary polyunsaturated fatty acids improve cholinergic transmission in the aged brain

2009

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The cholinergic theory of aging states that dysfunction of cholinergic neurons arising from the basal forebrain and terminating in the cortex and hippocampus may be involved in the cognitive decline that occurs during aging and Alzheimer's disease. Despite years of research, pharmacological interventions to treat or forestall the development of Alzheimer's disease have primarily focused on enhancing cholinergic transmission, either through increasing acetylcholine (ACh) synthesis or inhibition of the acetylcholinesterase enzyme responsible for ACh hydrolysis. However, recent studies have indicated that dietary supplementation can impact the cholinergic system, particularly during aging. The purpose of the present review is to examine the relevant research suggesting that cholinergic functioning may be maintained during aging via consuming a diet containing polyunsaturated fatty acids (PUFAs). The data reviewed herein indicate that, at least in animal studies, inclusion of PUFAs in the diet can improve cholinergic transmission in the brain, possibly leading to improvements in cognitive functioning.

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“…Increased membrane PS levels were found in neuroblastoma cells supplemented with DHA [70]. Shahdat et al [71] demonstrated that DHA administered orally significantly increased rat brain phospholipid content. Dietary enrichment with a specific combination of membrane precursors and cofactors (DHA, EPA, uridine, choline, folate, vitamin B 12 , vitamin B 6 , phospholipids, vitamin C, vitamin E, and selenium, i.e., FC) also increased neuronal membrane PC levels in the intracerebroventricular (ICV) A␤-infused rat model of AD [72].…”

Section: Precursor Control Of Membrane Formationmentioning

confidence: 98%

Targeting Synaptic Dysfunction in Alzheimer's Disease by Administering a Specific Nutrient Combination

Wijk

Broersen

Wilde

et al. 2013

JAD

107

101

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Synapse loss and synaptic dysfunction are pathological processes already involved in the early stages of Alzheimer's disease (AD). Synapses consist principally of neuronal membranes, and the neuronal and synaptic losses observed in AD have been linked to the degeneration and altered composition and structure of these membranes. Consequently, synapse loss and membrane-related pathology provide viable targets for intervention in AD. The specific nutrient combination Fortasyn Connect (FC) is designed to ameliorate synapse loss and synaptic dysfunction in AD by addressing distinct nutritional needs believed to be present in these patients. This nutrient combination comprises uridine, docosahexaenoic acid, eicosapentaenoic acid, choline, phospholipids, folic acid, vitamins B12, B6, C, and E, and selenium, and is present in Souvenaid, a medical food intended for use in early AD. It has been hypothesized that FC counteracts synaptic loss and reduces membrane-related pathology in AD by providing nutritional precursors and cofactors that act together to support neuronal membrane formation and function. Preclinical studies formed the basis of this hypothesis which is being validated in a broad clinical study program investigating the potential of this nutrient combination in AD. Memory dysfunction is one key early manifestation in AD and is associated with synapse loss. The clinical studies to date show that the FC-containing medical food improves memory function and preserves functional brain network organization in mild AD compared with controls, supporting the hypothesis that this intervention counteracts synaptic dysfunction. This review provides a comprehensive overview of basic scientific studies that led to the creation of FC and of its effects in various preclinical models.

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Synaptic plasma membrane-bound acetylcholinesterase activity is not affected by docosahexaenoic acid-induced decrease in membrane order

Cited by 23 publications

References 58 publications

The protective effect of dietary eicosapentaenoic acid against impairment of spatial cognition learning ability in rats infused with amyloid β(1–40)

The protective effect of dietary eicosapentaenoic acid against impairment of spatial cognition learning ability in rats infused with amyloid β(1–40)

Dietary polyunsaturated fatty acids improve cholinergic transmission in the aged brain

Targeting Synaptic Dysfunction in Alzheimer's Disease by Administering a Specific Nutrient Combination

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