scholarly journals The influence of diet patterns on Alzheimer’s risk: a concise systematic review

2021 ◽  
Vol 14 (3) ◽  
Author(s):  
Sayonara Carrijo Machado ◽  
Idiberto José Zotarelli Filho
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorder ◽  
Cognitive Disorders ◽  
Health Concern ◽  
Eating Patterns ◽  
Diet Patterns ◽  
Age Related ◽  
Neurochemical Changes ◽  
The Relationship ◽  
Over Time

Alzheimer's disease (AD) is a progressive neurodegenerative disorder responsible for the main cause of dementia, and the increasing worldwide prevalence of AD is a major public health concern. Studies suggest that diet and nutrition may be important modifiable risk factors for AD. In addition, intestinal microbial metabolites and their effects on host neurochemical changes can increase or decrease the risk of AD. The aim of this literature review article is to discuss the relationship between dietary patterns, foods, gut microbiota, micro and macronutrients, and cognitive disorders, especially Alzheimer's. The results show that the excessive generation and accumulation of reactive pro-oxidant species over time can damage proteins, lipids, carbohydrates, and nucleic acids. Over time, this oxidative stress can contribute to a variety of age-related degenerative diseases. Therefore, antioxidant foods and healthy eating patterns, such as the Mediterranean diet, can contribute to reducing oxidative stress and consequently reducing the risk of Alzheimer's.

scholarly journals Lost in a Dream

2019 ◽  
pp. 381-396
Author(s):  
Carlos L. Rodriguez ◽  
Babak Tousi
Keyword(s):  
Motor Neurons ◽  
Neurodegenerative Disorders ◽  
Dementia With Lewy Bodies ◽  
Neurodegenerative Disorder ◽  
Lewy Bodies ◽  
Behavior Disorder ◽  
Sleep Behavior ◽  
The Relationship ◽  
Over Time

Rapid-eye-movement sleep behavior disorder (RBD) is a parasomnia that is closely associated with neurodegenerative disorders. RBD is usually caused by neurodegeneration within the brainstem that disables the system responsible for immobilizing skeletal muscles during REM sleep and thus permits motor neurons to activate these muscles during dreaming. The underlying source of the brainstem neurodegeneration spreads over time to other central nervous system regions until it has sufficiently evolved to permit clinical recognition of the underlying neurodegenerative disorder. Longitudinal follow-up of patients with RBD has demonstrated that most patients subsequently develop some neurodegenerative disorder years later, particularly the synucleinopathies. We review the relationship between RBD and dementia with Lewy bodies, which is one of the synucleinopathies. The management of RBD is reviewed with discussion of the relevant considerations in patients with dementia with Lewy bodies.

scholarly journals The Triggering Receptor Expressed on Myeloid Cells 2: “TREM-ming” the Inflammatory Component Associated with Alzheimer's Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Troy T. Rohn
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Neurodegenerative Disorder ◽  
Late Onset ◽  
Senile Plaques ◽  
Myeloid Cells ◽  
Disease Process ◽  
Age Related

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by a progressive loss of memory and cognitive skills. Although much attention has been devoted concerning the contribution of the microscopic lesions, senile plaques, and neurofibrillary tangles to the disease process, inflammation has long been suspected to play a major role in the etiology of AD. Recently, a novel variant in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) has been identified that has refocused the spotlight back onto inflammation as a major contributing factor in AD. Variants in TREM2 triple one's risk of developing late-onset AD. TREM2 is expressed on microglial cells, the resident macrophages in the CNS, and functions to stimulate phagocytosis on one hand and to suppress cytokine production and inflammation on the other hand. The purpose of this paper is to discuss these recent developments including the potential role that TREM2 normally plays and how loss of function may contribute to AD pathogenesis by enhancing oxidative stress and inflammation within the CNS. In this context, an overview of the pathways linking beta-amyloid, neurofibrillary tangles (NFTs), oxidative stress, and inflammation will be discussed.

scholarly journals Metformin Alleviates Obesity and Systemic Oxidative Stress in Obese Young Swine

2020 ◽  
Vol 13 (7) ◽  
pp. 142
Author(s):  
Susana Astiz ◽  
Antonio Gonzalez-Bulnes ◽  
Isabel Astiz ◽  
Alicia Barbero ◽  
Jose Luis Pesantez-Pacheco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Status ◽  
Swine Model ◽  
Oxygen Species ◽  
Systemic Oxidative Stress ◽  
Age Related ◽  
Cardiometabolic Disorders ◽  
Iberian Pig ◽  
The Relationship ◽  
Related Increase

The present study assessed the relationship between obesity induced by lifestyle and systemic oxidative stress and possible modulations by oral metformin treatments in young individuals, by using a translational swine model of obesity and associated cardiometabolic disorders (Iberian pig). The results indicate the existence of an age-related increase in both adiposity and systemic oxidative stress (using hydrogen peroxide as a marker), which is higher in individuals with obesogenic lifestyle and increased weight and obesity. Such effect was not found in individuals treated with metformin. The translation of these results suggests that childhood obesity increases production of reactive oxygen species (ROS), and therefore systemic oxidative stress. Treatment with metformin would improve such oxidative status.

Amyotrophic Lateral Sclerosis Disease and Environmental Risk Factors

2019 ◽  
pp. 286-304
Author(s):  
Abdeljalil Elgot ◽  
Hasna Lahouaoui ◽  
Ouassil El Kherchi ◽  
Nadia Zouhairi
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Heavy Metals ◽  
Amyotrophic Lateral Sclerosis ◽  
Genetic Background ◽  
Neurodegenerative Disorder ◽  
Neurodegenerative Process ◽  
Peripheral Motor ◽  
The Relationship ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that affects central and peripheral motor neuron cells leading to a severe muscle weakness. Until now, no efficient cures exist and those existing are limited. The ALS etiology remains obscure, although the relationship between genetic background and environmental insults including pesticides and heavy metals is well documented. These latter may play a major role in the onset of the ALS neurodegenerative process. Pesticides are known to have many benefits to mankind in the agricultural and industrial areas, but their toxicities in humans have always been a debatable issue. The pathophysiological mechanisms involve, among others, inflammation processes, oxidative stress, and mitochondrial function impairments. The aim of this chapter was to examine the association between the risk of amyotrophic lateral sclerosis (ALS) and exposure to pesticides and heavy metals.

scholarly journals FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2/HO-1 Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-21 ◽  
Author(s):  
Ting Wan ◽  
Zihao Wang ◽  
Yi Luo ◽  
Yifan Zhang ◽  
Wei He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Caffeic Acid ◽  
Cell Apoptosis ◽  
Nuclear Translocation ◽  
Neurodegenerative Disorder ◽  
Neuronal Cell ◽  
Caffeic Acid Phenethyl Ester ◽  
Therapeutic Drug ◽  
Age Related

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder with cognitive deficits, which is becoming markedly more common in the world. Currently, the exact cause of AD is still unclear, and no curative therapy is available for preventing or mitigating the disease progression. Caffeic acid phenethyl ester (CAPE), a natural phenolic compound derived from honeybee hive propolis, has been reported as a potential therapeutic agent against AD, while its application is limited due to the low water solubility and poor bioavailability. Here, caffeic acid phenethyl ester 4-O-glucoside (FA-97) is synthesized. We validate that FA-97 attenuates H2O2-induced apoptosis in SH-SY5Y and PC12 cells and suppresses H2O2-induced oxidative stress by inhibiting the ROS level, malondialdehyde (MDA) level, and protein carbonylation level, as well as induces cellular glutathione (GSH) and superoxide dismutase (SOD). Mechanistically, FA-97 promotes the nuclear translocation and transcriptional activity of Nrf2 associated with the upregulated expression of HO-1 and NQO-1. The prime importance of Nrf2 activation in the neuroprotective and antioxidant effects of FA-97 is verified by Nrf2 siRNA transfection. In addition, FA-97 prevents scopolamine- (SCOP-) induced learning and memory impairments in vivo via reducing neuronal apoptosis and protecting against cholinergic system dysfunction in the hippocampus and cortex. Moreover, the increased MDA level and low total antioxidant capacity in SCOP-treated mouse brains are reversed by FA-97, with the increased expression of HO-1, NQO-1, and nuclear Nrf2. In conclusion, FA-97 protects against oxidative stress-mediated neuronal cell apoptosis and SCOP-induced cognitive impairment by activating Nrf2/HO-1 signaling, which might be developed as a therapeutic drug for AD.

scholarly journals Probiotics: An Adjuvant therapy for D-Galactose induced Alzheimer's disease

2017 ◽  
Vol 1 (1) ◽  
pp. 30-33 ◽  
Author(s):  
Varshil Mehta ◽  
Kavya Bhatt ◽  
Nimit Desai ◽  
Mansi Naik
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Brain Regions ◽  
Health Concern ◽  
Major Health ◽  
Acetyl Choline ◽  
Glycation End Products ◽  
Anti Oxidant

Alzheimer’s disease (AD) is a chronic and slowly progressing neurodegenerative disorder which has become a major health concern worldwide. The literature has shown that oxidative stress is one of the most important risk factors behind the cause of AD. Oxidative stress often leads to the production of Reactive Oxygen Species (ROS). D-Galactose, a physiological nutrient and reducing sugar, non-enzymatically reacts with amines of amino acids in proteins and peptides to form Advanced Glycation End products which activate its receptors coupled to Biochemical pathways that stimulate free radical production and induces mitochondrial dysfunction which damages the neuron intracellularly. High dosage of D-Galactose also suppresses the expression of nerve growth factors and its associated protein which results in the degeneration of nerve cells and reduction of acetylcholine levels in brain regions. This article put forwards the advantages of using Lactic Acid Bacteria (Probiotics) possessing anti-oxidant properties and which produces Acetyl Choline against D-Galactose induced Alzheimer’s disease.

scholarly journals THE RELATIONSHIP BETWEEN OLDER DRIVERS’ RESILIENCE AND SELF-REPORTED DRIVING MEASURES OVER 5 YEARS

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S344-S344
Author(s):  
Renée M St Louis ◽  
Judith Charlton ◽  
Sjaan Koppel ◽  
Lisa J Molnar ◽  
Marilyn Di Stefano ◽  
...  
Keyword(s):  
Older Drivers ◽  
Future Research ◽  
Driving Frequency ◽  
Older Adulthood ◽  
Resilience Scale ◽  
Age Related ◽  
Positive Correlations ◽  
Changes Over Time ◽  
The Relationship ◽  
Over Time

Abstract As people age into older adulthood, they are more likely to experience events that impact their driving, such as age-related cognitive and functional declines, serious illness, or disability. The ability to demonstrate resilience following such adversity may influence one’s decisions and feelings about driving. This study investigated whether resilience of older drivers changes over time, and if relationships between resilience, gender, and self-reported driving-related abilities, perceptions and practices remain stable or change. Participants were from the Candrive/Ozcandrive study, a prospective cohort study of older drivers from Canada, Australia and New Zealand. Analyses are presented from a subset of Ozcandrive participants (n=125) from Australia who completed a resilience scale at two time points approximately five years apart, as well as measures of driving comfort during the day and night, perceived driving abilities, and driving frequency. Participants were primarily male (67.2%) with a mean age of 81.6 years (SD=3.3, Range=76.0-90.0) at Time 1. Resilience increased significantly from Time 1 to Time 2 (Median=82.0/84.00, z=-2.9, p<.01). Although females had significantly higher resilience than males at both Time 1 (Median=84.0/81.0, U=2.3, p=.02) and Time 2 (Median=86.5/82.0, U=2.1, p=.03), there was a statistically significant increase in resilience of males over five years (p<.01) and no statistical change for females. Results show small but significant positive correlations, and increasingly stronger relationships over time between older drivers’ resilience and driving comfort as well as perceived driving abilities. Future research will use modelling to examine the association of various factors on the change in resilience and driving-related measures.

scholarly journals Curcumin Effectively Rescued Parkinson’s Disease-Like Phenotypes in a Novel Drosophila melanogaster Model with dUCH Knockdown

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Thi Thanh Nguyen ◽  
My Dung Vuu ◽  
Man Anh Huynh ◽  
Masamitsu Yamaguchi ◽  
Linh Thuoc Tran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Genetic Factors ◽  
Neurodegenerative Disorder ◽  
Appropriate Therapy ◽  
Genetic And Environmental Factors ◽  
The Relationship ◽  
Common Neurodegenerative Disorder

The relationship between oxidative stress and neurodegenerative diseases has been extensively examined, and antioxidants are considered to be a promising approach for decelerating disease progression. Parkinson’s disease (PD) is a common neurodegenerative disorder and affects 1% of the population over 60 years of age. A complex combination of genetic and environmental factors contributes to the pathogenesis of PD. However, since the onset mechanisms of PD have not yet been elucidated in detail, difficulties are associated with developing effective treatments. Curcumin has been reported to have neuroprotective properties in PD models induced by neurotoxins or genetic factors such as α-synuclein, PINK1, DJ-1, and LRRK2. In the present study, we investigated the effects of curcumin in a novel Drosophila model of PD with knockdown of dUCH, a homolog of human UCH-L1. We found that dopaminergic neuron-specific knockdown of dUCH caused impaired movement and the loss of dopaminergic neurons. Furthermore, the knockdown of dUCH induced oxidative stress while curcumin decreased the ROS level induced by this knockdown. In addition, dUCH knockdown flies treated with curcumin had improved locomotive abilities and less severe neurodegeneration. Taken together, with studies on other PD models, these results strongly suggest that treatments with curcumin are an appropriate therapy for PD related to oxidative stress.

scholarly journals Age-Related Oxidative Changes in Primary Porcine Fibroblasts Expressing Mutated Huntingtin

2019 ◽  
Vol 19 (1) ◽  
pp. 22-34
Author(s):  
Petra Smatlikova ◽  
Georgina Askeland ◽  
Michaela Vaskovicova ◽  
Jiri Klima ◽  
Jan Motlik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Nuclear Dna ◽  
Neurodegenerative Disorder ◽  
Cyclin B1 ◽  
Gene Encoding ◽  
Proliferation Capacity ◽  
Mitochondrial Superoxide ◽  
Age Related ◽  
The Impact

Background: Huntington’s disease (HD) is a devastating neurodegenerative disorder caused by CAG triplet expansions in the huntingtin gene. Oxidative stress is linked to HD pathology, although it is not clear whether this is an effect or a mediator of disease. The transgenic (TgHD) minipig expresses the N-terminal part of human-mutated huntingtin and represents a unique model to investigate therapeutic strategies towards HD. A more detailed characterization of this model is needed to fully utilize its potential. Methods: In this study, we focused on the molecular and cellular features of fibroblasts isolated from TgHD minipigs and the wild-type (WT) siblings at different ages, pre-symptomatic at the age of 24–36 months and with the onset of behavioural symptoms at the age of 48 months. We measured oxidative stress, the expression of oxidative stress-related genes, proliferation capacity along with the expression of cyclin B1 and D1 proteins, cellular permeability, and the integrity of the nuclear DNA (nDNA) and mitochondrial DNA in these cells. Results: TgHD fibroblasts isolated from 48-month-old animals showed increased oxidative stress, which correlated with the overexpression of SOD2 encoding mitochondrial superoxide dismutase 2, and the NEIL3 gene encoding DNA glycosylase involved in replication-associated repair of oxidized DNA. TgHD cells displayed an abnormal proliferation capacity and permeability. We further demonstrated increased nDNA damage in pre-symptomatic TgHD fibroblasts (isolated from animals aged 24–36 months). Conclusions: Our results unravel phenotypic alterations in primary fibroblasts isolated from the TgHD minipig model at the age of 48 months. Importantly, nDNA damage appears to precede these phenotypic alterations. Our results highlight the impact of fibroblasts from TgHD minipigs in studying the molecular mechanisms of HD pathophysiology that gradually occur with age.

scholarly journals Relationship between Oxidative Stress, Circadian Rhythms, and AMD

2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
María Luisa Fanjul-Moles ◽  
Germán Octavio López-Riquelme
Keyword(s):  
Oxidative Stress ◽  
Circadian Rhythms ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Retinal Damage ◽  
Cell Organelles ◽  
Age Related ◽  
Exogenous Factors ◽  
The Relationship

This work reviews concepts regarding oxidative stress and the mechanisms by which endogenous and exogenous factors produce reactive oxygen species (ROS). It also surveys the relationships between oxidative stress, circadian rhythms, and retinal damage in humans, particularly those related to light and photodamage. In the first section, the production of ROS by different cell organelles and biomolecules and the antioxidant mechanisms that antagonize this damage are reviewed. The second section includes a brief review of circadian clocks and their relationship with the cellular redox state. In the third part of this work, the relationship between retinal damage and ROS is described. The last part of this work focuses on retinal degenerative pathology, age-related macular degeneration, and the relationships between this pathology, ROS, and light. Finally, the possible interactions between the retinal pigment epithelium (RPE), circadian rhythms, and this pathology are discussed.

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