Neuronutrition and Alzheimer's Disease

Ramesh, B N; Rao, T.S. Sathyanarayana; Prakasam, A.; Sambamurti, Kumar; Rao, K. S.

doi:10.3233/jad-2010-1312

Cited by 92 publications

(51 citation statements)

References 196 publications

(202 reference statements)

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“…Importantly, toxicity in C. elegans ND models is influenced by the insulin pathway [(8, 9, 16, 47) and our own unpublished observations] providing a link between food source and proteotoxicity. Although the differences between the nematode and human diet are obvious, our observation is consistent with an increasing number of studies that support a role of environmental factors, such as diet and environmental toxins, in ND (52,53,73).…”

supporting

confidence: 89%

Protective Role of DNJ-27/ERdj5 inCaenorhabditis elegansModels of Human Neurodegenerative Diseases

Muñoz-Lobato

Rodríguez-Palero

Naranjo-Galindo

et al. 2014

Antioxidants & Redox Signaling

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Aims: Cells have developed quality control systems for protection against proteotoxicity. Misfolded and aggregation-prone proteins, which are behind the initiation and progression of many neurodegenerative diseases (ND), are known to challenge the proteostasis network of the cells. We aimed to explore the role of DNJ-27/ ERdj5, an endoplasmic reticulum (ER)-resident thioredoxin protein required as a disulfide reductase for the degradation of misfolded proteins, in well-established Caenorhabditis elegans models of Alzheimer, Parkinson and Huntington diseases. Results: We demonstrate that DNJ-27 is an ER luminal protein and that its expression is induced upon ER stress via IRE-1/XBP-1. When dnj-27 expression is downregulated by RNA interference we find an increase in the aggregation and associated pathological phenotypes (paralysis and motility impairment) caused by human b-amyloid peptide (Ab), a-synuclein (a-syn) and polyglutamine (polyQ) proteins. In turn, DNJ-27 overexpression ameliorates these deleterious phenotypes. Surprisingly, despite being an ER-resident protein, we show that dnj-27 downregulation alters cytoplasmic protein homeostasis and causes mitochondrial fragmentation. We further demonstrate that DNJ-27 overexpression substantially protects against the mitochondrial fragmentation caused by human Ab and a-syn peptides in these worm models. Innovation: We identify C. elegans dnj-27 as a novel protective gene for the toxicity associated with the expression of human Ab, a-syn and polyQ proteins, implying a protective role of ERdj5 in Alzheimer, Parkinson and Huntington diseases. Conclusion: Our data support a scenario where the levels of DNJ-27/ERdj5 in the ER impact cytoplasmic protein homeostasis and the integrity of the mitochondrial network which might underlie its protective effects in models of proteotoxicity associated to human ND. Antioxid. Redox Signal. 20,[217][218][219][220][221][222][223][224][225][226][227][228][229][230][231][232][233][234][235]

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supporting

confidence: 89%

Protective Role of DNJ-27/ERdj5 inCaenorhabditis elegansModels of Human Neurodegenerative Diseases

Muñoz-Lobato

Rodríguez-Palero

Naranjo-Galindo

et al. 2014

Antioxidants & Redox Signaling

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“…Interestingly, there has been increasing support for diet playing a role in AD (4)(5)(6). A number of dietary factors such as saturated fatty acids, higher calorie intake, and excessive alcohol (7) have been reported to increase the risk of dementia and AD (8). In particular, a number of studies have shown the close association of alcoholic consumption and dementia, although the exact mechanisms are still not known (9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic alcohol consumption on expression levels of APP and Aβ-producing enzymes

Kim¹,

Jeong²,

Yang³

et al. 2011

BMB Reports

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Chronic alcohol consumption contributes to numerous diseases, including cancers, cardiovascular diseases, and liver cirrhosis. Epidemiological studies have shown that excessive alcohol consumption is a risk factor for dementia. Along this line, Alzheimer's disease (AD) is the most common form of dementia and is caused by the accumulation of amyloid-β (Aβ plaques in neurons. In this study, we hypothesized that chronic ethanol consumption is associated with pathological processing of APP in AD. To investigate the relationship between chronic alcohol consumption and Aβ production, brain samples from rats fed an alcohol liquid diet for 5 weeks were analyzed. We show that the expression levels of APP, BACE1, and immature nicastrin were increased in the cerebellum, hippocampus, and striatum of the alcohol-fed group compared to the control group. Total nicastrin and PS1 levels were induced in the hippocampus of alcohol-fed rats. These data suggest that the altered expression of APP and Aβ-producing enzymes possibly contributes to the chronic alcohol consumption-mediated pathogenesis of AD. [BMB reports 2011; 44(2): 135-139]

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“…Red wine contains at least 19 types of polyphenols; among these, resveratrol is the most abundant 13 . Thus, the beneficial effect of wine on neurodegeneration can be attributed to resveratrol 10 .…”

Section: Main Conclusionmentioning

confidence: 99%

“…Since then, it has been increasing exponentially, and it is now considered a 21 st century epidemic, affecting approximately 26 million people worldwide and one quarter of the people aged above 85 years [8][9][10][11] .…”

Section: Alzheimer's Disease: the Dimension Of The Problemmentioning

confidence: 99%

“…Therefore, when motivated and supported by health professionals, individuals can use lifestyle options to influence their late-life cognitive performance and risk of brain disorders 10,15,26 . Among these options, nutrition has drawn much attention as a growing amount of evidence suggests that it may be a key factor in the development of Alzheimer's disease 10,24 .…”

Section: Alzheimer's Disease Risk and Protective Factorsmentioning

confidence: 99%

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Prevention of Alzheimer's disease: The role of the Mediterranean diet

Sousa

Guimarães

2015

Rev. Nutr.

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Rev. Nutr., Campinas, 28(6):691-703, nov./dez., 2015 Revista de Nutrição A B S T R A C TAlzheimer's disease rates have been increasing exponentially and are now considered a 21 st century epidemic. It contributes substantially to the morbidity and mortality of older adults. Thus, Alzheimer's disease is a growing major public health concern with a profuse socioeconomic impact. In addition, the existing pharmacological agents only offer modest symptomatic relief and can neither address the progressive neurodegeneration nor cure the disease. Therefore, finding effective preventive and therapeutic measures that delay the onset or reverse the course of the disease is crucial. Several studies have shown that lifestyle factors may play a central role in reducing the risk of developing Alzheimer's disease or, at least, in delaying its clinical symptoms. Among these disease-modifying factors, healthy nutrition has drawn much attention given that it might strongly influence the risk of cognitive decline, dementia, and Alzheimer's disease. Such healthy dietary pattern is the Mediterranean diet. The Mediterranean diet may play a protective role against age-related changes in cognitive function, pre-dementia syndromes, and dementia. Therefore, it may constitute an effective preventive strategy for Alzheimer's disease, with low costs and few side effects. Importantly, these promising preventive measures may translate into strong epidemiological health outcomes, which might lead to a significant progress in public health. An online search was conducted in PubMed in order to revise the literature concerning the association between diet and dementia, specifically, if a higher adherence to the Mediterranean diet pattern is related to lower risk of developing Alzheimer's disease, and to understand the possible mechanisms that may explain such association.Keywords: Alzheimer disease. Diet. Mediterranean diet. Prevention. R E S U M O I N T R O D U C T I O NSince its first description in the beginning of the XX century, Alzheimer's disease has gone from a rarely reported disorder to one of the most frequent causes of disability in older adults. Accordingly, cognitive decline and particularly Alzheimer's disease are major contributors to morbidity and mortality worldwide. Numerous studies performed in the last decades have given essential insights into the nature of Alzheimer's disease and importantly, into the magnitude of the problem. However, research on Alzheimer's disease is still an endless challenge, particularly in the area of prevention 1 .Since the times of Ancient Greece, lifestyle modifications, such as diet and exercise, can recognizably prevent or even treat several diseases, a concept that is well reflected on the well-known Hippocratic saying, "Let food be your medicine, let medicine be your food" (p.1295) 2 . Recently, many efforts have been made to describe the association between diet and cognitive function given that several studies have reported that nutrient intake and dietary practices strongly influence the...

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Neuronutrition and Alzheimer's Disease

Cited by 92 publications

References 196 publications

Protective Role of DNJ-27/ERdj5 inCaenorhabditis elegansModels of Human Neurodegenerative Diseases

Protective Role of DNJ-27/ERdj5 inCaenorhabditis elegansModels of Human Neurodegenerative Diseases

Effects of chronic alcohol consumption on expression levels of APP and Aβ-producing enzymes

Prevention of Alzheimer's disease: The role of the Mediterranean diet

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