Dietary Fatty Acid Factors in Alzheimer’s Disease: A Review

2020 ◽  
Vol 78 (3) ◽  
pp. 887-904
Author(s):  
Tianying Zhang ◽  
Xiaojuan Han ◽  
Xiaohua Zhang ◽  
Zhi Chen ◽  
Yajing Mi ◽  
...  

Alzheimer’s disease (AD) is an irreversible neurodegenerative disease characterized by brain function disorder and chronic cognitive function impairment. The onset of AD is complex and is mostly attributed to interactions between genetic factors and environmental factors. Lifestyle, dietary habits, and food consumption are likely to play indispensable functions in aged-related neurodegenerative diseases in elderly people. An increasing number of epidemiological studies have linked dietary fatty acid factors to AD, raising the point of view that fatty acid metabolism plays an important role in AD initiation and progression as well as in other central nervous system disorders. In this paper, we review the effects of the consumption of various dietary fatty acids on AD onset and progression and discuss the detrimental and beneficial effects of some typical fatty acids derived from dietary patterns on the pathology of AD. We outline these recent advances, and we recommend that healthy dietary lifestyles may contribute to preventing the occurrence and decreasing the pathology of AD.

The aging population is a significant social, medical and economic problem due to increasing prevalence of chronic diseases in elderly population. Alzheimer's disease (AD) is the most common form of dementia and the most common neurodegenerative disease. It is characterized by a progressive deterioration of memory and cognitive function. So far, there is neither an effective prevention nor cure for dementia, so more and more attention is paid to the prevention of this group of diseases, particularly to the appropriate diet. Preventive intervention gives the best results if introduced before the first symptoms of dementia, i.e., around the age of 50. This is when the nutritional status, number of synapses, cognition, and neuropathological changes in the nervous system compensate each other, which increases the chances of staying healthy for a longer period of time. It has been proven that dietary habits, which lead to the development of cardiovascular and metabolic diseases, significantly increase the risk of dementia. On the other hand, a Mediterranean diet rich in antioxidants, fiber and omega-3 polyunsaturated fatty acids may have a protective effect on the neurodegenerative process. The beneficial effect of many nutrients on the course of AD has been demonstrated. These include: glutathione, polyphenols, curcumin, coenzyme Q10, vitamins B6, B12, folic acid, unsaturated fatty acids, lecithin, UA, caffeine and some probiotic bacteria. A diet rich in saturated fatty acids and branched-chain amino acids (BCAA) promotes the progression of dementia. Dietary intervention should be introduced as early as possible to minimize the risk of developing dementia. The Mediterranean and DASH diets have been documented to protect against AD. However, the MIND diet is reported to be much more effective in preventing cognitive decline/dementia than either the Mediterranean or DASH diets alone.


2020 ◽  
Vol 11 (6) ◽  
pp. 1489-1509
Author(s):  
Tetsumori Yamashima ◽  
Tsuguhito Ota ◽  
Eishiro Mizukoshi ◽  
Hiroyuki Nakamura ◽  
Yasuhiko Yamamoto ◽  
...  

Abstract Although excessive consumption of deep-fried foods is regarded as 1 of the most important epidemiological factors of lifestyle diseases such as Alzheimer's disease, type 2 diabetes, and obesity, the exact mechanism remains unknown. This review aims to discuss whether heated cooking oil-derived peroxidation products cause cell degeneration/death for the occurrence of lifestyle diseases. Deep-fried foods cooked in ω-6 PUFA-rich vegetable oils such as rapeseed (canola), soybean, sunflower, and corn oils, already contain or intrinsically generate “hydroxynonenal” by peroxidation. As demonstrated previously, hydroxynonenal promotes carbonylation of heat-shock protein 70.1 (Hsp70.1), with the resultant impaired ability of cells to recycle damaged proteins and stabilize the lysosomal membrane. Until now, the implication of lysosomal/autophagy failure due to the daily consumption of ω-6 PUFA-rich vegetable oils in the progression of cell degeneration/death has not been reported. Since the “calpain-cathepsin hypothesis” was formulated as a cause of ischemic neuronal death in 1998, its relevance to Alzheimer's neuronal death has been suggested with particular attention to hydroxynonenal. However, its relevance to cell death of the hypothalamus, liver, and pancreas, especially related to appetite/energy control, is unknown. The hypothalamus senses information from both adipocyte-derived leptin and circulating free fatty acids. Concentrations of circulating fatty acid and its oxidized form, especially hydroxynonenal, are increased in obese and/or aged subjects. As overactivation of the fatty acid receptor G-protein coupled receptor 40 (GPR40) in response to excessive or oxidized fatty acids in these subjects may lead to the disruption of Ca2+ homeostasis, it should be evaluated whether GPR40 overactivation contributes to diverse cell death. Here, we describe the molecular implication of ω-6 PUFA-rich vegetable oil-derived hydroxynonenal in lysosomal destabilization leading to cell death. By oxidizing Hsp70.1, both the dietary PUFA- (exogenous) and the membrane phospholipid- (intrinsic) peroxidation product “hydroxynonenal,” when combined, may play crucial roles in the occurrence of diverse lifestyle diseases including Alzheimer's disease.


2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Daniel W. Nuno ◽  
Kathryn G. Lamping

Sphingolipids, modified by dietary fatty acids, are integral components of plasma membrane and caveolae that are also vasoactive compounds. We hypothesized that dietary fatty acid saturation affects vasoconstriction to sphingosine-1-phosphate (S1P) through caveolar regulation of rho kinase. Wild type (WT) and caveolin-1-deficient (cav-1 KO) mice which lack vascular caveolae were fed a low-fat diet (LF), 60% high-saturated fat diet (lard, HF), or 60% fat diet with equal amounts of lard and n-3 polyunsaturated menhaden oil (MO). Weight gain of WT on HF and MO diets was similar while markedly blunted in cav-1 KO. Neither high-fat diet affected the expression of cav-1, rho, or rho kinase in arteries from WT. In cav-1 KO, MO increased the vascular expression of rho but had no effect on rho kinase. HF had no effect on rho or rho kinase expression in cav-1 KO. S1P produced a concentration-dependent constriction of gracilis arteries from WT on LF that was reduced with HF and restored to normal with MO. Constriction to S1P was reduced in cav-1 KO and no longer affected by a high-saturated fat diet. Inhibition of rho kinase which reduced constriction to PE independent of diet in arteries from WT and cav-1 KO only reduced constriction to S1P in arteries from WT fed MO. The data suggest that dietary fatty acids modify vascular responses to S1P by a caveolar-dependent mechanism which is enhanced by dietary n-3 polyunsaturated fats.


2021 ◽  
Vol 10 (10) ◽  
pp. e450101018968
Author(s):  
Séfura Maria Assis Moura ◽  
Selene Maia de Morais ◽  
José Osvaldo Beserra Carioca ◽  
Ana Livya Moreira Rodrigues ◽  
Daniela Ribeiro Alves ◽  
...  

Acetylcholine deficiency is a neurochemical characteristic of patients with clinical diagnosis of Alzheimer´s disease. Substances that inhibit the enzyme acetylcholinesterase, increasing levels of acetylcholine in the brain, are a promising form of treatment. Studies relate the use of omega-3 fatty acids in the treatment and prevention of Alzheimer's disease. The Northeast Region of Brazil has an enormous biological diversity and a wide variety of fish species. In this work, the oils of eleven species of marine fish found on the coast of Ceará, Brazil, were analyzed in relation to the fatty acid profile and the inhibitory activity of the enzyme acetylcholinesterase. Total lipids were extracted from fish samples by Folch metodology. The lipid extracts of the fish and industrialized fish oil, used for comparison, were esterified and fatty acid profiles were analyzed. The acetylcholinesterase inhibitory activity was measured quantitatively. The oils presented a high percentage of saturated fatty acids, which is a general characteristic of tropical fish. Oleic acid was the highest monounsaturated fatty acid. Oils of Scomberomorus cavalla, Lutjanus synagris and Haemulon plumieri presented expressive percentages of polyunsaturated fatty acids and the most potent anticholinesterase activities. This research showed the oils of S. cavalla, L. synagris and H. plumieri may be promising functional food products of active fatty acids as new therapies to treatment or prevention of Alzheimer's disease. The expressive concentration of unsaturated and polyunsaturated fatty acids together with their relevant anticholinesterase activity are characteristics of the importance of these fish oils.


2021 ◽  
Vol 11 ◽  
Author(s):  
Abigail R. Basson ◽  
Christy Chen ◽  
Filip Sagl ◽  
Ashley Trotter ◽  
Ilya Bederman ◽  
...  

With the epidemic of human obesity, dietary fats have increasingly become a focal point of biomedical research. Epidemiological studies indicate that high-fat diets (HFDs), especially those rich in long-chain saturated fatty acids (e.g., Western Diet, National Health Examination survey; NHANES ‘What We Eat in America’ report) have multi-organ pro-inflammatory effects. Experimental studies have confirmed some of these disease associations, and have begun to elaborate mechanisms of disease induction. However, many of the observed effects from epidemiological studies appear to be an over-simplification of the mechanistic complexity that depends on dynamic interactions between the host, the particular fatty acid, and the rather personalized genetics and variability of the gut microbiota. Of interest, experimental studies have shown that certain saturated fats (e.g., lauric and myristic fatty acid-rich coconut oil) could exert the opposite effect; that is, desirable anti-inflammatory and protective mechanisms promoting gut health by unanticipated pathways. Owing to the experimental advantages of laboratory animals for the study of mechanisms under well-controlled dietary settings, we focus this review on the current understanding of how dietary fatty acids impact intestinal biology. We center this discussion on studies from mice and rats, with validation in cell culture systems or human studies. We provide a scoping overview of the most studied diseases mechanisms associated with the induction or prevention of Inflammatory Bowel Disease in rodent models relevant to Crohn’s Disease and Ulcerative Colitis after feeding either high-fat diet (HFD) or feed containing specific fatty acid or other target dietary molecule. Finally, we provide a general outlook on areas that have been largely or scarcely studied, and assess the effects of HFDs on acute and chronic forms of intestinal inflammation.


2020 ◽  
Author(s):  
Prabir Khatua ◽  
Asis Jana ◽  
Ulrich H. E. Hansmann

AbstractWhile Alzheimer’s disease is correlated with the presence of Aβ fibrils in patient brains, the more likely agents are their precursors, soluble oligomers that may form pores or otherwise distort cell membranes. Using all-atom molecular dynamics simulation we study how presence of fatty acids such as lauric acid changes the stability of pore-forming oligomers built from three-stranded Aβ42 chains. Such a change would alter the distribution of amyloids in the fatty-acid rich brain environment, and therefore could explain the lower polymorphism observed in Aβ-fibrils derived from brains of patients with Alzheimer’s disease. We find that lauric acid stabilizes both ring-like and barrel-shaped models, with the effect being stronger for barrel-like models than for ring-like oligomers.


2014 ◽  
Vol 306 (12) ◽  
pp. E1388-E1396 ◽  
Author(s):  
Sébastien M. Labbé ◽  
Christophe Noll ◽  
Thomas Grenier-Larouche ◽  
Margaret Kunach ◽  
Lucie Bouffard ◽  
...  

Using a novel positron emission tomography (PET) method with oral administration of 14( R, S)-[18F]-fluoro-6-thia-heptadecanoic acid (18FTHA), we recently demonstrated that subjects with impaired glucose tolerance (IGT) display an impairment in cardiac function associated with increased myocardial uptake of dietary fatty acids. Here, we determined whether modest weight loss induced by lifestyle changes might improve these cardiac metabolic and functional abnormalities. Nine participants with IGT, enrolled in a one-year lifestyle intervention trial, were invited to undergo determination of organ-specific postprandial dietary fatty acids partition using the oral 18FTHA method, and cardiac function and oxidative metabolic index using PET [11C]acetate kinetics with ECG-gated PET ventriculography before and after the intervention. The intervention resulted in significant weight loss and reduction of waist circumference, with reduced postprandial plasma glucose, insulin, and triglycerides excursion. We observed a significant increase in stroke volume, cardiac output, and left ventricular ejection fraction associated with reduced myocardial oxidative metabolic index and fractional dietary fatty acid uptake. Modest weight loss corrects the exaggerated myocardial channeling of dietary fatty acids and improves myocardial energy substrate metabolism and function in IGT subjects.


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