scholarly journals Papel del estrés oxidativo en el desarrollo del deterioro cognitivo y su progresión a enfermedad de Alzheimer

2019 ◽  
pp. 14-22
Author(s):  
Josue CRUZ-RODRÍGUEZ ◽  
Gabriel BETANZOS-CABRERA ◽  
Brenda Hildeliza CAMACHO-DÍAZ ◽  
María Araceli ORTIZ-RODRÍGUEZ
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Free Radicals ◽  
Neuronal Death ◽  
Energy Demand ◽  
Brain Aging ◽  
Neurological Diseases ◽  
Amyloid Peptide

This review aims to provide scientific evidence of the role of oxidative stress in the development of cognitive impairment and its progression to Alzheimer's disease. Oxidative stress originates when there is an uncontrolled production of free radicals that disrupts the balance between oxidants and antioxidants, favoring oxidants. It has been associated with oxidative stress with the pathogenesis of brain aging, cognitive impairment and some neurological diseases. The cells of the central nervous system produce a high amount of free radicals since their energy demand is high, this coupled with a low antioxidant capacity, favors the appearance of a pro-oxidant environment that contributes to neurodegeneration and neuronal death. Alzheimer's disease is the most frequent form of dementia, it is characterized by neurodegenerative changes that occur with cognitive impairment, progressive impairment of memory and thought, until preventing the performance of daily life activities. Neuropathologically, it is characterized by the presence of extracellular deposits of β-amyloid peptide in the form of neurofibrillar plaques and clews; lesions capable of generating damage and neuronal death that lead to cognitive failure through the generation of more free radicals

scholarly journals Modulating Effect of Diet on Alzheimer’s Disease

Diseases ◽  
2019 ◽  
Vol 7 (1) ◽  
pp. 12 ◽  
Author(s):  
Paloma Fernández-Sanz ◽  
Daniel Ruiz-Gabarre ◽  
Vega García-Escudero
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Response ◽  
Scientific Evidence ◽  
Senile Plaques ◽  
Neuronal Loss ◽  
Pleiotropic Effect ◽  
Amyloid Peptide ◽  
Dietary Recommendations

As life expectancy is growing, neurodegenerative disorders, such as Alzheimer’s disease, are increasing. This disease is characterised by the accumulation of intracellular neurofibrillary tangles formed by hyperphosphorylated tau protein, senile plaques composed of an extracellular deposit of β-amyloid peptide (Aβ), and neuronal loss. This is accompanied by deficient mitochondrial function, increased oxidative stress, altered inflammatory response, and autophagy process impairment. The present study gathers scientific evidence that demonstrates that specific nutrients exert a direct effect on both Aβ production and Tau processing and their elimination by autophagy activation. Likewise, certain nutrients can modulate the inflammatory response and the oxidative stress related to the disease. However, the extent to which these effects come with beneficial clinical outcomes remains unclear. Even so, several studies have shown the benefits of the Mediterranean diet on Alzheimer’s disease, due to its richness in many of these compounds, to which can be attributed their neuroprotective properties due to the pleiotropic effect they show on the aforementioned processes. These indications highlight the potential role of adequate dietary recommendations for clinical management of both Alzheimer’s diagnosed patients and those in risk of developing it, emphasising once again the importance of diet on health.

scholarly journals Cancer Chemotherapy Related Cognitive Impairment and the Impact of the Alzheimer’s Disease Risk Factor APOE

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3842
Author(s):  
Harvey R. Fernandez ◽  
Ashima Varma ◽  
Sarah A. Flowers ◽  
George William Rebeck
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Cognitive Impairment ◽  
Blood Brain Barrier ◽  
Cancer Chemotherapy ◽  
Apoe Genotype ◽  
Brain Barrier ◽  
Blood Brain

Cancer related cognitive impairment (CRCI) is a serious impairment to maintaining quality of life in cancer survivors. Cancer chemotherapy contributes to this condition through several potential mechanisms, including damage to the blood brain barrier, increases in oxidative stress and inflammation in the brain, and impaired neurogenesis, each of which lead to neuronal dysfunction. A genetic predisposition to CRCI is the E4 allele of the Apolipoprotein E gene (APOE), which is also the strongest genetic risk factor for Alzheimer’s disease. In normal brains, APOE performs essential lipid transport functions. The APOE4 isoform has been linked to altered lipid binding, increased oxidative stress and inflammation, reduced turnover of neural progenitor cells, and impairment of the blood brain barrier. As chemotherapy also affects these processes, the influence of APOE4 on CRCI takes on great significance. This review outlines the main areas where APOE genotype could play a role in CRCI. Potential therapeutics based on APOE biology could mitigate these detrimental cognitive effects for those receiving chemotherapy, emphasizing that the APOE genotype could help in developing personalized cancer treatment regimens.

scholarly journals Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease

2004 ◽  
Vol 101 (7) ◽  
pp. 2070-2075 ◽  
Author(s):  
Roy G. Cutler ◽  
Jeremiah Kelly ◽  
Kristin Storie ◽  
Ward A. Pedersen ◽  
Anita Tammara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Aging ◽  
Cholesterol Metabolism

Oxidative stress in blood in Alzheimer's disease and mild cognitive impairment: A meta-analysis

2013 ◽  
Vol 59 ◽  
pp. 100-110 ◽  
Author(s):  
M. Schrag ◽  
C. Mueller ◽  
M. Zabel ◽  
A. Crofton ◽  
W.M. Kirsch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Meta Analysis

P3-483: Oxidative Stress Peripheral Biomarkers in Mild Cognitive Impairment and Alzheimer's Disease

2010 ◽  
Vol 6 ◽  
pp. e12-e12
Author(s):  
Tania Marcourakis ◽  
Nathalia B. Quaglio ◽  
Larissa H.L. Torres ◽  
Gisele T. Souza ◽  
Raphael C.T. Garcia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment

scholarly journals Inflammation and Insulin Resistance as Risk Factors and Potential Therapeutic Targets for Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Angeles Vinuesa ◽  
Carlos Pomilio ◽  
Amal Gregosa ◽  
Melisa Bentivegna ◽  
Jessica Presa ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Brain Aging ◽  
Therapeutic Targets ◽  
Low Grade ◽  
Increased Risk ◽  
The Impact

Overnutrition and modern diets containing high proportions of saturated fat are among the major factors contributing to a low-grade state of inflammation, hyperglycemia and dyslipidemia. In the last decades, the global rise of type 2 diabetes and obesity prevalence has elicited a great interest in understanding how changes in metabolic function lead to an increased risk for premature brain aging and the development of neurodegenerative disorders such as Alzheimer’s disease (AD). Cognitive impairment and decreased neurogenic capacity could be a consequence of metabolic disturbances. In these scenarios, the interplay between inflammation and insulin resistance could represent a potential therapeutic target to prevent or ameliorate neurodegeneration and cognitive impairment. The present review aims to provide an update on the impact of metabolic stress pathways on AD with a focus on inflammation and insulin resistance as risk factors and therapeutic targets.

scholarly journals Ingredients in Zijuan Pu’er Tea Extract Alleviate β-Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer’s Disease Likely through DAF-16

Molecules ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 729 ◽  
Author(s):  
Fangzhou Du ◽  
Lin Zhou ◽  
Yan Jiao ◽  
Shuju Bai ◽  
Lu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Protective Effect ◽  
Nuclear Translocation ◽  
Amyloid Β ◽  
Amyloid Peptide ◽  
C Elegans ◽  
Β Amyloid

Amyloid-β, one of the hallmarks of Alzheimer’s disease (AD), is toxic to neurons and can also cause brain cell death. Oxidative stress is known to play an important role in AD, and there is strong evidence that oxidative stress is associated with amyloid-β. In the present study we report the protective effect of Zijuan Pu’er tea water extract (ZTWE) and the mixture of main ingredients (+)-catechins, caffeine and procyanidin (MCCP) in ZTWE on β-amyloid-induced toxicity in transgenic Caenorhabditis elegans (C. elegans) CL4176 expressing the human Aβ1–42 gene. ZTWE, (+)-catechins, caffeine, procyanidin and MCCP delayed the β-amyloid-induced paralysis to different degrees. The MCCP treatment did not affect the transcript abundance of amyloid-β transgene (amy-1); however, Thioflavin T staining showed a significant decrease in Aβ accumulation compared to untreated worms. Further research using transgenic worms found that MCCP promoted the translocation of DAF-16 from cytoplasm to nucleus and increased the expression of superoxide dismutase 3 (SOD-3). In addition, MCCP decreased the reactive oxygen species (ROS) content and increased the SOD activity in CL4176 worms. In conclusion, the results suggested that MCCP had a significant protective effect on β-amyloid-induced toxicity in C. elegans by reducing β-amyloid aggregation and inducing DAF-16 nuclear translocation that could activate the downstream signal pathway and enhance resistance to oxidative stress.

Oxidative signalling and inflammatory pathways in Alzheimer's disease

2001 ◽  
Vol 67 ◽  
pp. 141-149 ◽  
Author(s):  
Ian Anderson ◽  
Christy Adinolfi ◽  
Susan Doctrow ◽  
Karl Huffman ◽  
Ken A. Joy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Cell ◽  
Amyloid Peptide ◽  
Microglial Cells ◽  
Amino Acid Form ◽  
Factor Α ◽  
Molecular Components ◽  
And Oxidative Stress

It is well established that inflammation and oxidative stress are key components of the pathology of Alzheimer's disease (AD), but how early in the pathological cascade these processes are involved or which specific molecular components are key, has not been fully elucidated. This paper describes the pharmacological approach to understand the molecular components of inflammation and oxidative stress on the activation of microglial cells and neuronal cell viability. We have shown that activation of microglia with the 42-amino-acid form of the ϐ-amyloid peptide (Aϐ42) activates the production of cyclooxygenase-2, the inducible form of nitric oxide synthase and tumour necrosis factor-α and there appears to be little interactive feedback between these three mediators. Moreover, we explore the effects of a series of salen-manganese complexes, EUK-8, -134 and -189, which are known to possess both superoxide and catalase activity. These compounds are able to protect cells from insults produced by hydrogen peroxide or peroxynitrite. Moreover, EUK-134 was also able to limit the output of prostaglandin E2 from activated microglial cells. The mechanisms underlying these effects are discussed. Together, these data support a pivotal role for oxidative stress and inflammation as key mediators of the pathological cascade in AD and provide some ideas about possible therapeutic targets.

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