scholarly journals Beneficial Effects on Brain Micro-Environment by Caloric Restriction in Alleviating Neurodegenerative Diseases and Brain Aging

2021 ◽  
Vol 12 ◽  
Author(s):  
Li Zhang ◽  
Huachong Xu ◽  
Ning Ding ◽  
Xue Li ◽  
Xiaoyin Chen ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Caloric Restriction ◽  
Metabolic Disorders ◽  
Brain Aging ◽  
Future Perspectives ◽  
Brain Health ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Extracellular Microenvironment

Aging and neurodegenerative diseases are frequently associated with the disruption of the extracellular microenvironment, which includes mesenchyme and body fluid components. Caloric restriction (CR) has been recognized as a lifestyle intervention that can improve long-term health. In addition to preventing metabolic disorders, CR has been shown to improve brain health owing to its enhancing effect on cognitive functions or retarding effect on the progression of neurodegenerative diseases. This article summarizes current findings regarding the neuroprotective effects of CR, which include the modulation of metabolism, autophagy, oxidative stress, and neuroinflammation. This review may offer future perspectives for brain aging interventions.

scholarly journals Long-Term Caloric Restriction Attenuates β-Amyloid Neuropathology and Is Accompanied by Autophagy in APPswe/PS1delta9 Mice

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 985
Author(s):  
Luisa Müller ◽  
Nicole Power Guerra ◽  
Jan Stenzel ◽  
Claire Rühlmann ◽  
Tobias Lindner ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Neuroprotective Effect ◽  
Resonance Spectroscopy ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Positron Emission ◽  
Pet Ct ◽  
Amyloid Aβ ◽  
Β Amyloid

Caloric restriction (CR) slows the aging process, extends lifespan, and exerts neuroprotective effects. It is widely accepted that CR attenuates β-amyloid (Aβ) neuropathology in models of Alzheimer’s disease (AD) by so-far unknown mechanisms. One promising process induced by CR is autophagy, which is known to degrade aggregated proteins such as amyloids. In addition, autophagy positively regulates glucose uptake and may improve cerebral hypometabolism—a hallmark of AD—and, consequently, neural activity. To evaluate this hypothesis, APPswe/PS1delta9 (tg) mice and their littermates (wild-type, wt) underwent CR for either 16 or 68 weeks. Whereas short-term CR for 16 weeks revealed no noteworthy changes of AD phenotype in tg mice, long-term CR for 68 weeks showed beneficial effects. Thus, cerebral glucose metabolism and neuronal integrity were markedly increased upon 68 weeks CR in tg mice, indicated by an elevated hippocampal fluorodeoxyglucose [18F] ([18F]FDG) uptake and increased N-acetylaspartate-to-creatine ratio using positron emission tomography/computer tomography (PET/CT) imaging and magnet resonance spectroscopy (MRS). Improved neuronal activity and integrity resulted in a better cognitive performance within the Morris Water Maze. Moreover, CR for 68 weeks caused a significant increase of LC3BII and p62 protein expression, showing enhanced autophagy. Additionally, a significant decrease of Aβ plaques in tg mice in the hippocampus was observed, accompanied by reduced microgliosis as indicated by significantly decreased numbers of iba1-positive cells. In summary, long-term CR revealed an overall neuroprotective effect in tg mice. Further, this study shows, for the first time, that CR-induced autophagy in tg mice accompanies the observed attenuation of Aβ pathology.

scholarly journals Caloric restriction mitigates age-associated hippocampal differential CG and non-CG methylation

2017 ◽  
Author(s):  
Niran Hadad ◽  
Archana Unnikrishnan ◽  
Jordan A. Jackson ◽  
Dustin R. Masser ◽  
Laura Otalora ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Caloric Restriction ◽  
Brain Aging ◽  
Regulatory Element ◽  
Memory Function ◽  
Promoter Hypermethylation ◽  
Epigenetic Mechanism ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Age Related

AbstractBrain aging is marked by cognitive decline and susceptibility to neurodegeneration. Caloric-restriction (CR) increases neurogenesis, improves memory function, and protects from age-associated neurological disorders. Epigenetic mechanisms, including DNA methylation, are vital to normal CNS cellular and memory functions, and are dysregulated with aging. The beneficial effects of CR have been proposed to work through epigenetic processes, but this is largely unexplored. We therefore tested whether life-long CR prevents age-related DNA methylation changes in the brain. Hippocampal DNA from young (3 months) and old (24 months) male mice fed ad libitum and 24 month old mice fed a 40% calorierestricted diet from 3 months of age were examined by genome-wide bisulfite sequencing to measure methylation with base-specificity. Over 27 million CG and CH (non-CG) sites were examined. Of the ~40,000 differentially methylated CGs (dmCGs) and ~80,000 CHs (dmCHs) with aging, >1/3 were prevented by CR and were found across genomic regulatory regions and gene pathways. CR also caused alterations to CG and CH methylation at sites not differentially methylated with aging, and these CR-specific changes demonstrated a different pattern of regulatory element and gene pathway enrichment than those affected by aging. CR-specific DNMT1 and TET3 promoter hypermethylation corresponded to reduced gene expression. These findings demonstrate that CR attenuates age-related CG and CH hippocampal methylation changes, in combination with CR-specific methylation that may also contribute to the neuroprotective effects of CR. The prevention of age-related methylation alterations is also consistent with the pro-longevity effects of CR working through an epigenetic mechanism.

The beneficial effects of Lactobacillus fermented black barley on high fat diet-induced fatty liver in rats

2021 ◽  
Author(s):  
Qi Guan ◽  
Xinwen Ding ◽  
Lingyue Zhong ◽  
Chuang Zhu ◽  
Pan Nie ◽  
...  
Keyword(s):  
Fatty Liver ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
High Fat ◽  
Beneficial Effects ◽  
Phytochemical Composition

Long term high-fat diet (HF) can cause metabolic disorders, which might induce fatty liver. Fermented whole cereal food exhibit healthy potential due to their unique phytochemical composition and probiotics. In...

scholarly journals Molecular and cellular pathways contributing to brain aging

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Aliabbas Zia ◽  
Ali Mohammad Pourbagher-Shahri ◽  
Tahereh Farkhondeh ◽  
Saeed Samarghandian
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Brain Aging ◽  
Neuroprotective Effect ◽  
Ros Generation ◽  
Brain Health ◽  
Cellular Pathways ◽  
Aging Mechanisms ◽  
Oxidatively Modified ◽  
Biology Of Aging

AbstractAging is the leading risk factor for several age-associated diseases such as neurodegenerative diseases. Understanding the biology of aging mechanisms is essential to the pursuit of brain health. In this regard, brain aging is defined by a gradual decrease in neurophysiological functions, impaired adaptive neuroplasticity, dysregulation of neuronal Ca2+ homeostasis, neuroinflammation, and oxidatively modified molecules and organelles. Numerous pathways lead to brain aging, including increased oxidative stress, inflammation, disturbances in energy metabolism such as deregulated autophagy, mitochondrial dysfunction, and IGF-1, mTOR, ROS, AMPK, SIRTs, and p53 as central modulators of the metabolic control, connecting aging to the pathways, which lead to neurodegenerative disorders. Also, calorie restriction (CR), physical exercise, and mental activities can extend lifespan and increase nervous system resistance to age-associated neurodegenerative diseases. The neuroprotective effect of CR involves increased protection against ROS generation, maintenance of cellular Ca2+ homeostasis, and inhibition of apoptosis. The recent evidence about the modem molecular and cellular methods in neurobiology to brain aging is exhibiting a significant potential in brain cells for adaptation to aging and resistance to neurodegenerative disorders.

Diet and Brain Health: Which Role for Polyphenols?

2018 ◽  
Vol 24 (2) ◽  
pp. 227-238 ◽  
Author(s):  
Vanessa Castelli ◽  
Davide Grassi ◽  
Raffaella Bocale ◽  
Michele d'Angelo ◽  
Andrea Antonosante ◽  
...  
Keyword(s):  
Cognitive Performance ◽  
Brain Aging ◽  
Experimental Studies ◽  
Brain Health ◽  
Lifestyle Modifications ◽  
Dietary Polyphenols ◽  
Beneficial Effects ◽  
The Central Nervous System ◽  
The Relationship

Background: The aging of western societies is leading to a dramatic increase in the prevalence of chronic conditions, threatening the health status and then the sustainability of our healthcare systems. In particular, dementia is being increasingly recognized as a public health priority, given its enormous socioeconomic burdens further amplified by the absence of treatments really effective in improving the clinical course of the disease. Methods: The question of whether some degree of cognitive deterioration is an inevitable part of aging or should be considered as a pathological pre-stage of dementia is currently debated. This is a field in need of research because accelerated brain aging as well as further decline in cognition might be preventable in the early stages of cognitive impairment. Herein, we discuss evidence from clinical and experimental studies on the role of polyphenols in preserving cognitive performance across life. Results: In recent years, the possibility of favorably influencing the cognitive trajectory through promotion of lifestyle modifications has been increasingly investigated. In particular, the relationship between nutritional habits and brain health has attracted special attention. Dietary polyphenols exhibit a strong potential to promote brain due to their efficacy in protecting neurons against oxidative stress-induced injury, suppressing neuroinflammation and in ameliorating cardiovascular risk factor control and cardiovascular function thus counteracting neurotoxicity and neurodegeneration. Conclusion: Emerging evidence suggest that dietary polyphenols, in particular flavonoids, may exert beneficial effects on the central nervous system thus representing a potential tool to preserve cognitive performance throught senescence.

scholarly journals Neuroprotective Effects of a Combined Therapy With Memantine, Donepezil and Vitamin D in Ovariectomized Female Mice Subjected to Dementia Model

2021 ◽  
Author(s):  
Ana Daniela Coutinho Vieira ◽  
Eduarda Behenck Medeiros ◽  
Gabriel Casagrande Zabot ◽  
Nathalia de Souza Pereira ◽  
Natália Baltazar do Nascimento ◽  
...  
Keyword(s):  
Vitamin D ◽  
Combined Therapy ◽  
Neuroprotective Effects ◽  
Female Mice ◽  
Beneficial Effects ◽  
Gfap Immunoreactivity ◽  
Short And Long Term ◽  
Triple Treatment ◽  
Inflammation Parameters

Abstract The postmenopausal period is characterized by a decrease in the hormonal supply which is associated with Alzheimer's Disease (AD). Vitamin D is neuroprotective and can be used in combination with pre-existing medications to improve its effects. The objective was to evaluate the effect of vitamin D associated with memantine and donepezil in female mice submitted to ovariectomy (OVX) for 5 months and subjected to an AD-induced dementia model. Animals were divided into 5 groups who received 17 days of treatment and were subjected to behavioral tests. The animals underwent euthanasia at 18th day. OVX groups exhibit reduced levels of E2 and triple treatment group had high levels of vitamin D. The induction of dementia with OVX induced short- and long-term spatial and habituation memories damage. Also, induced reduction of BDNF and IL-4 levels in hippocampus, and increasing levels of TNFα in hippocampus and of IL-1β in hippocampus and frontal cortex of animals, as well as a significant increase on GFAP immunoreactivity. Triple-association treatment reversed the effects of long-term spatial and habituation memories damage, as well as reversed changes in TNFα, IL-1β, IL-4 and GFAP immunoreactivity levels in hippocampus of treated animals. Therapeutic association has beneficial effects on memory and inflammation parameters in female mice subjected to OVX and the AD animal model of dementia.

scholarly journals Knowing Your Beans in Parkinson’s Disease: A Critical Assessment of Current Knowledge about Different Beans and Their Compounds in the Treatment of Parkinson’s Disease and in Animal Models

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Michel Rijntjes
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Models ◽  
Current Knowledge ◽  
Mucuna Pruriens ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Natural Therapy ◽  
Bioactive Ingredients

This review contains a critical appraisal of current knowledge about the use of beans in both animal models and patients with Parkinson’s disease (PD). The potential beneficial effects of beans in PD are increasingly being touted, not only in scientific journals but also by the lay media. While there is a long tradition in Ayurvedic medicine of prescribing extracts from Mucuna pruriens (MP), whose seeds contain 5% L-3,4-dihydroxyphenylalanin (L-DOPA), many other beans also contain L-DOPA (broad beans, common beans, and soybeans) or have other ingredients (coffee and cocoa) that may benefit PD patients. Indeed, bean-derived compounds can elicit neuroprotective effects in animal models of PD, while several studies in human PD patients have shown that motor performance can improve after ingestion of bean extracts. However, there are several arguments countering the view that beans serve as a natural therapy for PD: (i) the results from animal PD models are not necessarily directly applicable to humans; (ii) beans have many bioactive ingredients, some of which can be harmful in large doses; (iii) studies in human PD patients are scarce and only report on the effects of single doses or the administration of bean extract over short periods of time; and (iv) no data on long-term efficacy or side effects of bean therapy are available. Therefore, reservations about the use of beans as a “natural” therapy for PD seem to be justified.

scholarly journals Flavonoid-Rich Ethanol Extract from the Leaves of Diospyros kaki Attenuates D-Galactose-Induced Oxidative Stress and Neuroinflammation-Mediated Brain Aging in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yingjuan Ma ◽  
Bin Ma ◽  
Yuying Shang ◽  
Qingqing Yin ◽  
Dejie Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Nuclear Translocation ◽  
Brain Aging ◽  
Ethanol Extract ◽  
Neurological Impairment ◽  
Diospyros Kaki ◽  
Neuroprotective Effects ◽  
Age Related ◽  
Y Maze

Aging is a major factor that contributes to neurological impairment and neuropathological changes, such as inflammation, oxidative stress, neuronal apoptosis, and synaptic dysfunction. Flavonoids act as protective antioxidant and anti-inflammatory agents against various age-related neurodegenerative diseases. Here, we investigated the protective effect and mechanisms of the flavonoid-rich ethanol extract from the leaves of Diospyros kaki (FELDK) in the cortex and hippocampus of D-galactose- (gal-) aged mice. Our results showed that FELDK treatment restored memory impairment in mice as determined by the Y-maze and Morris water maze tests. FELDK decreased oxidative stress levels via inhibiting reactive oxygen species (ROS) and malondialdehyde (MDA) production and elevating antioxidative enzymes. FELDK also alleviated D-gal-induced neuroinflammation via suppressing the expression of advanced glycation end products (AGEs) and receptor for AGEs (RAGE) and activating microgliosis and astrocytosis, nuclear factor kappa B (NF-κB) nuclear translocation, and downstream inflammatory mediators. Moreover, FELDK inhibited the phosphatidylinositol 3-kinase (PI3K)/Akt and C-jun N-terminal kinase (JNK) apoptotic signaling pathways and ameliorated the impairment of synapse-related proteins. Hence, these results indicate that FELDK exerts neuroprotective effects on D-gal-induced brain aging. Thus, FELDK may be a potential therapeutic strategy for preventing and treating age-related neurodegenerative diseases such as Alzheimer’s disease.

Neurodegenerative diseases and Flavonoids: Special reference to kaempferol

2021 ◽  
Vol 20 ◽  
Author(s):  
Rahul ◽  
Yasir Hasan Siddique
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neuroprotective Effects ◽  
Major Health Problem ◽  
Beneficial Effects

: Neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, Huntington’s disease, Multiple Sclerosis and Ischemic stroke have become a major health problem worldwide. Pre-clinical studies have demonstrated the beneficial effects of flavonoids on neurodegenerative diseases and suggesting them to be used as therapeutic agents. Kaempferol is found in many plants such as tea, beans, broccoli,strawberriesand has neuroprotective effects against the development of many neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease and Huntington's disease. The present study summarizesthe neuroprotective effects of kaempferol in various models of neurodegenerative diseases. Kaempferol delays the initiation as well as the progression of neurodegenerative disorders by acting as a scavenger of free radicals and preserving the activity of various antioxidant enzymes. Kaempferolcan crossthe blood-brain barrier (BBB), and therefore results inan enhanced protective effect. The multi-target property of kaempferol makes it a potential dietary supplement in preventing and treating neurodegenerative diseases.

scholarly journals Caloric Restriction and the Nutrient-Sensing PGC-1αin Mitochondrial Homeostasis: New Perspectives in Neurodegeneration

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Daniele Lettieri Barbato ◽  
Sara Baldelli ◽  
Beatrice Pagliei ◽  
Katia Aquilano ◽  
Maria Rosa Ciriolo
Keyword(s):  
Neurodegenerative Diseases ◽  
Caloric Restriction ◽  
Mitochondrial Biogenesis ◽  
Dietary Intervention ◽  
Current Knowledge ◽  
Nutritional Intervention ◽  
Nutrient Sensing ◽  
Mitochondrial Activity ◽  
Beneficial Effects ◽  
And Function

Mitochondrial activity progressively declines during ageing and in many neurodegenerative diseases. Caloric restriction (CR) has been suggested as a dietary intervention that is able to postpone the detrimental aspects of aging as it ameliorates mitochondrial performance. This effect is partially due to increased mitochondrial biogenesis. The nutrient-sensing PGC-1αis a transcriptional coactivator that promotes the expression of mitochondrial genes and is induced by CR. It is believed that many of the mitochondrial and metabolic benefits of CR are due to increased PGC-1αactivity. The increase of PGC-1αis also positively linked to neuroprotection and its decrement has been involved in the pathogenesis of many neurodegenerative diseases. This paper aims to summarize the current knowledge about the role of PGC-1αin neuronal homeostasis and the beneficial effects of CR on mitochondrial biogenesis and function. We also discuss how PGC-1α-governed pathways could be used as target for nutritional intervention to prevent neurodegeneration.

Sign in / Sign up

Export Citation Format

Share Document