scholarly journals Micronutrients and Alzheimer's disease

2005 ◽  
Vol 64 (4) ◽  
pp. 565-570 ◽  
Author(s):  
Hannes B. Staehelin
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fruits And Vegetables ◽  
Brain Aging ◽  
Model Systems ◽  
Bioactive Substances ◽  
Balanced Diet ◽  
Key Factor ◽  
Major Factors

The current high life expectancy is overshadowed by neurodegenerative illnesses that lead to dementia and dependence. Alzheimer's disease (AD) is the most common of these conditions, and is considered to be a proteinopathy, with amyloid-β42 as a key factor, leading via a cascade of events to neurodegeneration. Major factors involved are oxidative stress, perturbed Ca homeostasis and impaired energy metabolism. Protection against oxidative stress by micronutrients (including secondary bioactive substances) has been shown in transgenic Alzheimer model systems to delay AD. Epidemiological evidence is less conclusive, but the vast majority of the evidence supports a protective effect on cognitive functions in old age and AD. Thus, a diet rich in fruits and vegetables but also containing meat and fish is the most suitable to provide adequate micronutrients. The strong link between cardiovascular risk and AD may be explained by common pathogenetic mechanisms mediated, for example, by homocysteine and thus dependant on B-vitamins (folate and vitamins B12 and B6). However, micronutrients may also be harmful. The high affinity of amyloid for metals (Fe, Al and Zn) favours the generation of reactive oxygen species and triggers an inflammatory response. Micronutrients in a balanced diet have a long-lasting, albeit low, protective impact on brain aging, hence prevention should be life long.

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

scholarly journals Preventive Role of L-Carnitine and Balanced Diet in Alzheimer’s Disease

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1987
Author(s):  
Alina Kepka ◽  
Agnieszka Ochocinska ◽  
Małgorzata Borzym-Kluczyk ◽  
Ewa Skorupa ◽  
Beata Stasiewicz-Jarocka ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mediterranean Diet ◽  
Fruits And Vegetables ◽  
Brain Structures ◽  
Carnitine Deficiency ◽  
Processed Meat ◽  
Balanced Diet ◽  
The Mediterranean ◽  
The Mind

The prevention or alleviation of neurodegenerative diseases, including Alzheimer’s disease (AD), is a challenge for contemporary health services. The aim of this study was to review the literature on the prevention or alleviation of AD by introducing an appropriate carnitine-rich diet, dietary carnitine supplements and the MIND (Mediterranean-DASH Intervention for Neurodegenerative Delay) diet, which contains elements of the Mediterranean diet and the Dietary Approaches to Stop Hypertension (DASH) diet. L-carnitine (LC) plays a crucial role in the energetic metabolism of the cell. A properly balanced diet contains a substantial amount of LC as well as essential amino acids and microelements taking part in endogenous carnitine synthesis. In healthy people, carnitine biosynthesis is sufficient to prevent the symptoms of carnitine deficiency. In persons with dysfunction of mitochondria, e.g., with AD connected with extensive degeneration of the brain structures, there are often serious disturbances in the functioning of the whole organism. The Mediterranean diet is characterized by a high consumption of fruits and vegetables, cereals, nuts, olive oil, and seeds as the major source of fats, moderate consumption of fish and poultry, low to moderate consumption of dairy products and alcohol, and low intake of red and processed meat. The introduction of foodstuffs rich in carnitine and the MIND diet or carnitine supplementation of the AD patients may improve their functioning in everyday life.

scholarly journals The Effect of Kaempferol on Autophagy and Nrf-2 Signaling in a Rat Model of Aβ1-42-induced Alzheimer’s Disease

2022 ◽  
Vol 8 (1) ◽  
pp. 7-16
Author(s):  
Adeleh Jafari ◽  
◽  
Parvin Babaei ◽  
Kambiz Rohampour ◽  
Samira Rashtiani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Passive Avoidance ◽  
Rat Model ◽  
Natural Antioxidants ◽  
Beclin 1 ◽  
Key Factor ◽  
Male Wistar Rats ◽  
Avoidance Memory

Background: Numerous pieces of evidence support that oxidative stress is a key factor in the pathogenesis of neurodegenerative diseases, like Alzheimer’s Disease (AD). Suppression of oxidative stress is an attractive strategy and flavonoids as potent natural antioxidants are extremely noticeable. Objectives: In this study, the effects of Kaempferol (KMP) were evaluated on passive avoidance memory, hippocampal Nrf-2, and beclin-1 expression in a rat model of Aβ1-42 –induced AD. Materials & Methods: Forty male Wistar rats weighing 200-250 g were divided into five groups (n=8); sham-operated, AD model, and KMP treatment (5, 7.5, 10 mg/kg, i.p. for three weeks). Animals received an intracerebroventricular injection of amyloid-beta (1-42) to establish an AD model. Passive avoidance memory of rats was evaluated using a shuttle box on day 21; Step-Through Latency (STL) and time spent in The Dark Compartment (TDC) were recorded. Then, hippocampus homogenates were used for biochemical and molecular analysis by real-time PCR, western blot, and ELISA. Results: It was found that KMP improved memory evidenced by increased STL (P≤0.05) and decreased TDC (p≤0.01). KMP also increased the levels of Total Antioxidant Capacity (TAC) in the hippocampus of rats (P≤0.05). In addition, KMP enhanced the expression of Nrf-2 mRNA (P≤0.001) and beclin-1 protein in the hippocampus tissues (P≤0.001). Conclusion: Overall, it is suggested that the memory-improving effect of KMP is mediated, at least in part, by enhancing Nrf-2 and TAC. KMP is also able to induce autophagy through the expression of beclin-1.

scholarly journals A Long Journey into Aging, Brain Aging, and Alzheimer’s Disease Following the Oxidative Stress Tracks1

2018 ◽  
Vol 62 (3) ◽  
pp. 1319-1335 ◽  
Author(s):  
Patrizia Mecocci ◽  
Virginia Boccardi ◽  
Roberta Cecchetti ◽  
Patrizia Bastiani ◽  
Michela Scamosci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Aging ◽  
Aging Brain

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

Elevated oxidative stress in models of normal brain aging and Alzheimer's disease

Life Sciences ◽  
1999 ◽  
Vol 65 (18-19) ◽  
pp. 1883-1892 ◽  
Author(s):  
D.Allan Butterfield ◽  
Beverly Howard ◽  
Servet Yatin ◽  
Tanuja Koppal ◽  
Jennifer Drake ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Aging ◽  
Normal Brain

scholarly journals Gingko biloba Extract (EGb) Inhibits Oxidative Stress in Neuro 2A Cells Overexpressing APPsw

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Le Chen ◽  
Chenghong Zhang ◽  
Ying Han ◽  
Xianyi Meng ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Radicals ◽  
Early Event ◽  
Gingko Biloba ◽  
Empty Vector ◽  
Key Factor ◽  
And Control ◽  
Human Wild Type

Alzheimer’s disease (AD) is a common neurodegenerative disease. Abundant evidence demonstrates that oxidative stress may be not only an early event in this disease, but also a key factor in the pathogenesis of AD. Ginkgo biloba extract (EGb) has a strong ability to scavenge oxygen free radicals and supply hydrogen. The present study aims to investigate the effects of EGb on Neuro 2A cells transfected with Swedish mutant APP (APPsw). Stably transfected Neuro 2A cell lines expressing human wild-type APP (APP695), APPsw, or empty vector(neo) pEGFP-N2 were treated with 100 μg/ml EGb for 0, 2, 4, 6, 8, and 10 h. Oxidative stress was assessed by measuring free radicals and the activities of antioxidant enzymes. Our studies showed that EGb treatment reduced the production of reactive oxygen species (ROS) and the levels of malondialdehyde (MDA) significantly while total superoxide dismutase (T-SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were enhanced in Neuro 2A cells overexpressing APPsw. Meanwhile, Aβ levels in these cells were also reduced compared to the levels in untreated cells and control cells (empty vector(neo) pEGFP-N2). These findings suggest that EGb can reduce oxidative stress by decreasing free radical and enhancing antioxidant status, further leading to reduced Aβ aggregation; EGb might be a potential therapeutic agent for Alzheimer’s disease (AD).

Longitudinal Changes in Individual BrainAGE in Healthy Aging, Mild Cognitive Impairment, and Alzheimer’s Disease

GeroPsych ◽  
2012 ◽  
Vol 25 (4) ◽  
pp. 235-245 ◽  
Author(s):  
Katja Franke ◽  
Christian Gaser
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Healthy Aging ◽  
Brain Aging ◽  
Elderly Subjects ◽  
Additional Increase ◽  
Longitudinal Changes ◽  
Novel Method ◽  
The Brain

We recently proposed a novel method that aggregates the multidimensional aging pattern across the brain to a single value. This method proved to provide stable and reliable estimates of brain aging – even across different scanners. While investigating longitudinal changes in BrainAGE in about 400 elderly subjects, we discovered that patients with Alzheimer’s disease and subjects who had converted to AD within 3 years showed accelerated brain atrophy by +6 years at baseline. An additional increase in BrainAGE accumulated to a score of about +9 years during follow-up. Accelerated brain aging was related to prospective cognitive decline and disease severity. In conclusion, the BrainAGE framework indicates discrepancies in brain aging and could thus serve as an indicator for cognitive functioning in the future.

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