scholarly journals Intake of ω-6 Polyunsaturated Fatty Acid-Rich Vegetable Oils and Risk of Lifestyle Diseases

2020 ◽  
Vol 11 (6) ◽  
pp. 1489-1509
Author(s):  
Tetsumori Yamashima ◽  
Tsuguhito Ota ◽  
Eishiro Mizukoshi ◽  
Hiroyuki Nakamura ◽  
Yasuhiko Yamamoto ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Cell Death ◽  
Fatty Acid ◽  
Vegetable Oils ◽  
Neuronal Death ◽  
Cell Degeneration ◽  
Fried Foods ◽  
Lifestyle Diseases

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.

scholarly journals Fatty acids profile and anticholinesterase activity of fish lipids from Brazilian Northeast

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 ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Inhibitory Activity ◽  
Biological Diversity ◽  
Tropical Fish ◽  
Anticholinesterase Activity ◽  
Fish Samples

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.

scholarly journals Effect of Lauric Acid on the Stability of Aβ42-Oligomers

2020 ◽  
Author(s):  
Prabir Khatua ◽  
Asis Jana ◽  
Ulrich H. E. Hansmann
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Dynamics ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Molecular Dynamics Simulation ◽  
Lauric Acid ◽  
Cell Membranes ◽  
Dynamics Simulation ◽  
The Stability

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.

scholarly journals Mechanisms of Neuronal Death in the Cerebral Cortex during Aging and Development of Alzheimer’s Disease-Like Pathology in Rats

2019 ◽  
Vol 20 (22) ◽  
pp. 5632 ◽  
Author(s):  
Darya V. Telegina ◽  
Gleb K. Suvorov ◽  
Oyuna S. Kozhevnikova ◽  
Nataliya G. Kolosova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Decision Making ◽  
Cell Death ◽  
Cerebral Cortex ◽  
Brain Development ◽  
Brain Region ◽  
Neuronal Death ◽  
Neuronal Loss ◽  
Decision Making Behavior

Alzheimer’s disease (AD) is the commonest type of late-life dementia and damages the cerebral cortex, a vulnerable brain region implicated in memory, emotion, cognition, and decision-making behavior. AD is characterized by progressive neuronal loss, but the mechanisms of cell death at different stages of the disease remain unknown. Here, by means of OXYS rats as an appropriate model of the most common (sporadic) AD form, we studied the main pathways of cell death during development of AD-like pathology, including the preclinical stage. We found that apoptosis is activated at the pre-symptomatic stage (age 20 days) correlating with the retardation of brain development in the OXYS strain early in life. Progression of the AD-like pathology was accompanied by activation of apoptosis and necroptosis resulting from a decline of autophagy-mediated proteostasis. Our results are consistent with the idea that the nature of changes in the pathways of apoptosis, autophagy, and necrosis depends on the stage of AD.

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 ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Dietary Habits ◽  
Epidemiological Studies ◽  
Point Of View ◽  
Dietary Fatty Acids ◽  
Dietary Fatty Acid ◽  
Beneficial Effects

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.

Nutritional aspects and their influences on the pathophysiology of

2014 ◽  
Vol 23 (1) ◽  
pp. 33
Author(s):  
Nathalia Liberato Nascimento ◽  
Iwyson Henrique Fernandes da Costa ◽  
Rivelilson Mendes de Freitas
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Folic Acid ◽  
Saturated Fatty Acids ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
High Intake ◽  
Neuroprotective Effects ◽  
Nutritional Factors

The objective of this study was to conduct a review about the nutritional aspects and their influences on the pathophysiology of Alzheimer’s disease. The review describes the pathophysiology of Alzheimer’s disease, the generally indicated diets, and the nutritional factors that may aggravate the disease based on a literature review using the following keywords in English and Portuguese: “Alzheimer’s disease”, “physiopathology”, “nutritional aspects”, and “antioxidants”. A total of 100 articles were found, 48 in Lilacs and 52 in MedLine, but only 54 articles were selected for the review. The use of antioxidants as free radical scavengers is generally indicated in diets for Alzheimer’s patients. Studies also suggest that caffeine, vitamin B12, and folic acid have neuroprotective effects. Cohort studies found that a high intake of saturated fatty acids and obesity increase the risk of Alzheimer’s disease. People with Alzheimer’s disease should avoid diets high in carbohydrates and saturated fats, and prefer foods high in antioxidants.Keywords: Alzheimer disease; Antioxidants; Neurophysiology; Review literture as topic.

p35 Deficiency Accelerates HMGB-1-mediated Neuronal Death in the Early Stages of an Alzheimer’s disease Mouse Model

2013 ◽  
Vol 10 (8) ◽  
pp. 829-843 ◽  
Author(s):  
Ahram Jang ◽  
Hyunjeong Liew ◽  
Yun-Mi Kim ◽  
Heesoon Choi ◽  
Saeromi Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Neuronal Death ◽  
Early Stages

Is it All Said for NSAIDs in Alzheimer’s Disease? Role of Mitochondrial Calcium Uptake

2018 ◽  
Vol 15 (6) ◽  
pp. 504-510 ◽  
Author(s):  
Sara Sanz-Blasco ◽  
Maria Calvo-Rodríguez ◽  
Erica Caballero ◽  
Monica Garcia-Durillo ◽  
Lucia Nunez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Amyloid Β ◽  
Epidemiological Data ◽  
Amyloid Β Peptide ◽  
Aβ Oligomers ◽  
Mitochondrial Potential ◽  
Disease Modifying Drugs ◽  
Definitive Evidence

Objectives: Epidemiological data suggest that non-steroidal anti-inflammatory drugs (NSAIDs) may protect against Alzheimer's disease (AD). Unfortunately, recent trials have failed in providing compelling evidence of neuroprotection. Discussion as to why NSAIDs effectivity is uncertain is ongoing. Possible explanations include the view that NSAIDs and other possible disease-modifying drugs should be provided before the patients develop symptoms of AD or cognitive decline. In addition, NSAID targets for neuroprotection are unclear. Both COX-dependent and independent mechanisms have been proposed, including γ-secretase that cleaves the amyloid precursor protein (APP) and yields amyloid β peptide (Aβ). Methods: We have proposed a neuroprotection mechanism for NSAIDs based on inhibition of mitochondrial Ca2+ overload. Aβ oligomers promote Ca2+ influx and mitochondrial Ca2+ overload leading to neuron cell death. Several non-specific NSAIDs including ibuprofen, sulindac, indomethacin and Rflurbiprofen depolarize mitochondria in the low µM range and prevent mitochondrial Ca2+ overload induced by Aβ oligomers and/or N-methyl-D-aspartate (NMDA). However, at larger concentrations, NSAIDs may collapse mitochondrial potential (ΔΨ) leading to cell death. Results: Accordingly, this mechanism may explain neuroprotection at low concentrations and damage at larger doses, thus providing clues on the failure of promising trials. Perhaps lower NSAID concentrations and/or alternative compounds with larger dynamic ranges should be considered for future trials to provide definitive evidence of neuroprotection against AD.

scholarly journals NLRP3 Inflammasome: A Starring Role in Amyloid-β- and Tau-Driven Pathological Events in Alzheimer’s Disease

2021 ◽  
pp. 1-22
Author(s):  
Mariana Van Zeller ◽  
Diogo M. Dias ◽  
Ana M. Sebastião ◽  
Cláudia A. Valente
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glial Cells ◽  
Neurofibrillary Tangles ◽  
Nlrp3 Inflammasome ◽  
Neuronal Death ◽  
Inflammatory Responses ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Wide Range

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease commonly diagnosed among the elderly population. AD is characterized by the loss of synaptic connections, neuronal death, and progressive cognitive impairment, attributed to the extracellular accumulation of senile plaques, composed by insoluble aggregates of amyloid-β (Aβ) peptides, and to the intraneuronal formation of neurofibrillary tangles shaped by hyperphosphorylated filaments of the microtubule-associated protein tau. However, evidence showed that chronic inflammatory responses, with long-lasting exacerbated release of proinflammatory cytokines by reactive glial cells, contribute to the pathophysiology of the disease. NLRP3 inflammasome (NLRP3), a cytosolic multiprotein complex sensor of a wide range of stimuli, was implicated in multiple neurological diseases, including AD. Herein, we review the most recent findings regarding the involvement of NLRP3 in the pathogenesis of AD. We address the mechanisms of NLRP3 priming and activation in glial cells by Aβ species and the potential role of neurofibrillary tangles and extracellular vesicles in disease progression. Neuronal death by NLRP3-mediated pyroptosis, driven by the interneuronal tau propagation, is also discussed. We present considerable evidence to claim that NLRP3 inhibition, is undoubtfully a potential therapeutic strategy for AD.

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