Environmental and dietary risk factors in Alzheimer’s disease

Dosunmu, Remi; Wu, Jinfang; Basha, Riyaz; Zawia, Nasser H.

doi:10.1586/14737175.7.7.887

Cited by 96 publications

(49 citation statements)

References 154 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These include, but are not limited to, pesticides (such as DDT), metals, and air pollution (Dosunmu et al, 2007). The heavy metal lead (Pb) still poses a danger as an environmental toxicant.…”

Section: Introductionmentioning

confidence: 99%

Developmental exposure to lead (Pb) alters the expression of the human tau gene and its products in a transgenic animal model

et al. 2016

View full text Add to dashboard Cite

Tauopathies are a class of neurodegenerative diseases associated with the pathological aggregationof the tau protein in the human brain. The best known of these illnesses is Alzheimer's disease (AD); a disease where the microtubule associated protein tau (MAPT) becomes hyperphosphorylated (lowering its binding affinity to microtubules) and aggregates within neurons in the form of neurofibrillary tangles (NFTs). In this paper we examine whether environmental factors play a significant role in tau pathogenesis. Our studies were conducted in a double mutant mouse model that expressed the human tau gene and lacked the gene for murine tau. The human tau mouse model was tested for the transgene's ability to respond to an environmental toxicant. Pups were developmentally exposed to lead (Pb) from postnatal day (PND) 1-20 with 0.2% Pb acetate. Mice were then sacrificed at PND 20, 30, 40 and 60. Protein and mRNA levels for tau and CDK5 as well as tau phosphorylation at Ser396 were determined. In addition, the potential role of miRNA in tau expression was investigated by measuring levels of miR-34c, a miRNA that targets the mRNA for human tau, at PND20 and 50. The expression of the human tau transgene was altered by developmental exposure to Pb. This exposure also altered the expression of miR-34c. Our findings are the first of their kind to test the responsiveness of the human tau gene to an environmental toxicant and to examine an epigenetic mechanism that may be involved in the regulation of this gene's expression.

show abstract

Section: Introductionmentioning

confidence: 99%

Developmental exposure to lead (Pb) alters the expression of the human tau gene and its products in a transgenic animal model

et al. 2016

View full text Add to dashboard Cite

show abstract

“…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).…”

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

View full text Add to dashboard Cite

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]

show abstract

“…Indeed, onecarbon metabolism alteration and consequent methylation reactions unbalance (i.e. loss of methyl groups) during aging represents one of the mechanisms by which environmental and dietary factors can promote LOAD [71][72][73][74][75]. Methyl nutrients participate in one-carbon metabolism and an imbalance of this metabolism could affect DNA methylation, an important mechanism for epigenetic control of gene expression, along with redox homeostasis impairment.…”

Section: Involvement Of Sam In Oxidative Stress and Neurodegenerationmentioning

confidence: 99%

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Cavallaro¹,

Fuso²,

D’Erme³

et al. 2016

Int J Clin Nutr Diet

View full text Add to dashboard Cite

S-adenosyl-L-methionine (SAM) is the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. SAM level in the organism decreases with aging and restoring the original levels through exogenous supplementation is an important tool for the improvement of many vital functions. Indeed, SAM deficiency may contribute to the onset of several diseases, i.e. depression, liver diseases, osteoarthritis and senile neurological disorders such as Alzheimer's and Parkinson's diseases. Recent evidences indicate that SAM may have an involvement in oxidative stress, a process which typically involves an alteration of cellular sulfur amino acids homeostasis. SAM is not only the principal methyl donor, but also a precursor of glutathione, the major endogenous antioxidant, whose role in counteracting oxidative stress is well known. In this review we will highlight the role of SAM not just as a methyl-donor but also as a regulator of different metabolic pathways involved in the antioxidant response in brain related disorders. Role of S-adenosylmethionine in the Modulation of Oxidative StressRelated Neurodegeneration Review ArticleOpen Access IntroductionThe interaction between environmental and genetic factors plays a fundamental role in inducing and modulating the aging processes towards brain disorders. Among environmental factors, diet and nutritional lifestyle have a key role in brain health through the alteration of the intake or the bioavailability of metabolites and cofactors. Specific nutritional factors have particular impact on one-carbon metabolism, which is a complex biochemical pathway regulated by the presence of folate, vitamin B12 and B6 (among other metabolites) and leading to the production of S-adenosyl-L-methionine (SAM), the main biological methyl donor in transmethylation reactions, consisting in the transferring of a methyl moiety to different substrates including DNA, proteins, lipids and RNA. This metabolism involves three interrelated biochemical pathways: folate cycle, transsulfuration pathway and methionine cycle. These three metabolic sequences were first combined and correlated in 1964 by Laster's group [1][2][3] giving the integrated point of view of transmethylation and transsulfuration pathways, linking sulfur amino acid metabolism to the provision of methyl groups for many biochemical processes. Normal functioning of this metabolic cycle is essential for growth and development and impairment of this metabolism; transmethylation efficiency is associated with many diseases like cardiovascular diseases [4][5], liver diseases [6-9], neural tube defects [10] and brain diseases [11][12][13][14][15][16]. One-carbon metabolism alterations, low methylation and oxidative stress are all linked to Late Onset Alzheimer's Disease (LOAD) [17][18][19][20][21][22][23][24] Moreover, wide confirmed reports underline the role of SAM dependent reactions in age related neurodegeneration also showi...

show abstract

Environmental and dietary risk factors in Alzheimer’s disease

Cited by 96 publications

References 154 publications

Developmental exposure to lead (Pb) alters the expression of the human tau gene and its products in a transgenic animal model

Developmental exposure to lead (Pb) alters the expression of the human tau gene and its products in a transgenic animal model

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

Role of S-adenosylmethionine in the Modulation of Oxidative Stress- Related Neurodegeneration

Contact Info

Product

Resources

About