Ingredients for Functional Drinks in Neurodegenerative Diseases: A Review

Several studies have indicated that oxidative stress is a major risk factor for the initiation and progression of neurological disorders like Parkinson's disease (PD) and Alzheimer's (AD). Therefore, reducing oxidative stress appears to be a rational choice for the prevention and reduction in the rate of progression of these neurological disorders. The brain utilizes about 25% of respired oxygen even though it represents only 5% of the body weight. Free radicals are generated during the normal intake of oxygen, during infection, and during normal oxidative metabolism of certain substrates. Although experimental data are consistent in demonstrating the neuroprotective effects of antioxidants in vitro and in animal models, the clinical evidence that antioxidant agents may prevent or slow the course of these diseases is still relatively unsatisfactory, and insufficient to strongly modify clinical practice. In this paper, natural possible substances that could be added to a beverage to prevent or decrease the developing of neurodegenerative diseases are reviewed.

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Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

International Journal of Molecular Sciences ◽

10.3390/ijms21072501 ◽

2020 ◽

Vol 21 (7) ◽

pp. 2501 ◽

Cited By ~ 2

Author(s):

Thomas Nury ◽

Gérard Lizard ◽

Anne Vejux

Keyword(s):

Oxidative Stress ◽

Fatty Acids ◽

Cell Death ◽

Neurodegenerative Diseases ◽

The Body ◽

Protein Accumulation ◽

Common Features ◽

Apoptosis And Inflammation ◽

The Brain ◽

And Oxidative Stress

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

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Biodiversity as a source of new pharmacophores: A new theory of memory III

Pure and Applied Chemistry ◽

10.1351/pac200577010075 ◽

2005 ◽

Vol 77 (1) ◽

pp. 75-81 ◽

Cited By ~ 6

Author(s):

◽

M. Iqbal Choudhary

Keyword(s):

Natural Products ◽

Anticancer Agents ◽

Neurological Disorders ◽

In Vitro Bioassay ◽

Natural Sources ◽

Chemical Basis ◽

Antioxidant Agents ◽

A Cell ◽

The Brain

Several classes of natural products with significant inhibitory activity against target enzymes involved in several diseases have been identified. Spectrophotometer and high-throughput assays were used to assess the inhibition of prolyl endopeptidase (PEP), which led us to some novel inhibitors having potential as anticancer agents. Inhibition of cholinesterase enzymes has led to the discovery of new inhibitors with potential for use in Alzheimer’s disease and other neurological disorders. We have also discovered several potent antioxidant agents from natural sources by using a battery of antioxidant assays. Anti-inflammatory activity of a number of natural products was assayed through a cell-based in vitro bioassay. This article also contains a section on a slightly different topic of chemical basis of memory as presented during the lecture. The theory of the chemical basis of memory based on hydrogen bonding in the brain is further elaborated.

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LongShengZhi Capsule Attenuates Alzheimer-Like Pathology in APP/PS1 Double Transgenic Mice by Reducing Neuronal Oxidative Stress and Inflammation

Frontiers in Aging Neuroscience ◽

10.3389/fnagi.2020.582455 ◽

2020 ◽

Vol 12 ◽

Author(s):

Zequn Yin ◽

Xuerui Wang ◽

Shihong Zheng ◽

Peichang Cao ◽

Yuanli Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Transgenic Mice ◽

Amyloid Β ◽

B Cell Lymphoma ◽

Acanthopanax Senticosus ◽

Neuroprotective Effects ◽

Long Term Treatment ◽

Double Transgenic Mice ◽

The Brain

Alzheimer’s disease (AD) is the most common form of dementia in the elderly. It may be caused by oxidative stress, inflammation, and cerebrovascular dysfunctions in the brain. LongShengZhi Capsule (LSZ), a traditional Chinese medicine, has been approved by the China Food and Drug Administration for treatment of patients with cardiovascular/cerebrovascular disease. LSZ contains several neuroprotective ingredients, including Hirudo, Astmgali Radix, Carthami Flos (Honghua), Persicae Semen (Taoren), Acori Tatarinowii Rhizoma (Shichangpu), and Acanthopanax Senticosus (Ciwujia). In this study, we aimed to determine the effect of LSZ on the AD process. Double transgenic mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1) to model AD were treated with LSZ for 7 months starting at 2 months of age. LSZ significantly improved the cognition of the mice without adverse effects, indicating its high degree of safety and efficacy after a long-term treatment. LSZ reduced AD biomarker Aβ plaque accumulation by inhibiting β-secretase and γ-secretase gene expression. LSZ also reduced p-Tau expression, cell death, and inflammation in the brain. Consistently, in vitro, LSZ ethanol extract enhanced neuronal viability by reducing L-glutamic acid-induced oxidative stress and inflammation in HT-22 cells. LSZ exerted antioxidative effects by enhancing superoxide dismutase and glutathione peroxidase expression, reduced Aβ accumulation by inhibiting β-secretase and γ-secretase mRNA expression, and decreased p-Tau level by inhibiting NF-κB-mediated inflammation. It also demonstrated neuroprotective effects by regulating the Fas cell surface death receptor/B-cell lymphoma 2/p53 pathway. Taken together, our study demonstrates the antioxidative stress, anti-inflammatory, and neuroprotective effects of LSZ in the AD-like pathological process and suggests it could be a potential medicine for AD treatment.

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Isomeric O-methyl cannabidiolquinones with dual BACH1/NRF2 activity

10.1101/2020.06.16.153981 ◽

2020 ◽

Author(s):

Laura Casares ◽

Juan Diego Unciti ◽

Maria Eugenia Prados ◽

Diego Caprioglio ◽

Maureen Higgins ◽

...

Keyword(s):

Oxidative Stress ◽

Multiple Sclerosis ◽

Neurodegenerative Diseases ◽

Cell Models ◽

Therapeutic Approaches ◽

Neuroprotective Effects ◽

Anti Oxidant ◽

Anti Inflammatory ◽

The Brain

ABSTRACTOxidative stress and inflammation in the brain are two key hallmarks of neurodegenerative diseases (NDs) such as Alzheimer’s, Parkinson’s, Huntington’s and multiple sclerosis. The axis NRF2-BACH1 has anti-inflammatory and anti-oxidant properties that could be exploited pharmacologically to obtain neuroprotective effects. Activation of NRF2 or inhibition of BACH1 are, individually, promising therapeutic approaches for NDs. Compounds with dual activity as NRF2 activators and BACH1 inhibitors, could therefore potentially provide a more robust antioxidant and anti-inflammatory effects, with an overall better neuroprotective outcome. The phytocannabinoid cannabidiol (CBD) inhibits BACH1 but lacks significant NRF2 activating properties. Based on this scaffold, we have developed a novel CBD derivative that is highly effective at both inhibiting BACH1 and activating NRF2. This new CBD derivative provides neuroprotection in cell models of relevance to Huntington’s disease, setting the basis for further developments in vivo.

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POTENTIAL USE OF SULFORAPHANE AS A NEUROPROTECTOR

Medical and Clinical Chemistry ◽

10.11603/mcch.2410-681x.2021.i2.12048 ◽

2021 ◽

pp. 125-136

Author(s):

S. A. Tsiumpala ◽

K. M. Starchevska ◽

V. I. Lushchak

Keyword(s):

Oxidative Stress ◽

Neurodegenerative Diseases ◽

Old Age ◽

Neurodegenerative Disorders ◽

Therapeutic Potential ◽

The Body ◽

Biologically Active ◽

Inflammatory Processes ◽

The Brain ◽

Potential Use

Introduction. Under normal conditions, oxidative stress and proinflammatory processes are tightly controlled. However, during neuroinflammation and overproduction of reactive oxygen species (ROS), homeostasis is disrupted, which may lead to development of Alzheimer’s disease, Parkinson’s disease and other neurodegenerative disorders. Inflammatory processes may result in neurodegenerative disorders. Sulforaphane is an isothiocyanate compound which has potential for treatment of neurodegenerative disorders. Its therapeutic potential is based on the ability to activate transcription of genes, that regulate protective cellular mechanisms. The importance of studying sulforaphane as a neuroprotector is based on the fact, that dementias are the seventh leading cause of death globally and actively progress due to aging of human population. In this review, the anti-inflammatory effects of sulforaphane in the brain and its use as a potential neuroprotector in the treatment of neurodegenerative diseases are discussed. The aim of the study – to review available literature sources on the potential use of sulforaphane to prevent or mitigate neuroinflammation. Conclusions. Economic and technological development of mankind and the improvement of the general quality of life leads to prolongation of human life. But, achievements of longevity give new challenges to humanity. In young age and early adulthood, the organisms can relatively easily maintain homeostasis, then in old age intensification of oxidative stress and inflammatory processes can lead to the development of dementias and mental disorders. What should we do now to save clear mind in old age? In this review, sulforaphane is considered to be a potential neuroprotector. Biologically active supplements and drugs containing sulforaphane can weaken up inflammatory processes in the brain and in the body in general, and therefore they can be used for prevention and treatment of neurodegenerative diseases.

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Antioxidant and Astroprotective Effects of aPulicaria incisaInfusion

Oxidative Medicine and Cellular Longevity ◽

10.1155/2012/157598 ◽

2012 ◽

Vol 2012 ◽

pp. 1-10 ◽

Cited By ~ 6

Author(s):

Anat Elmann ◽

Alona Telerman ◽

Sharon Mordechay ◽

Hilla Erlank ◽

Rivka Ofir

Keyword(s):

Oxidative Stress ◽

Neurodegenerative Diseases ◽

Brain Injuries ◽

Desert Plant ◽

Oxygen Species ◽

Intracellular Accumulation ◽

Glial Derived Neurotrophic Factor ◽

The Brain ◽

Antioxidant Effects

Oxidative stress is involved in the pathogenesis of neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support, such as glial-derived neurotrophic factor (GDNF). Thus, any damage to astrocytes will affect neuronal survival. In the present study, an infusion prepared from the desert plantPulicaria incisa(Pi) was tested for its protective and antioxidant effects on astrocytes subjected to oxidative stress. ThePiinfusion attenuated the intracellular accumulation of ROS following treatment with hydrogen peroxide and zinc and prevented the H2O2-induced death of astrocytes. ThePiinfusion also exhibited an antioxidant effectin vitroand induced GDNF transcription in astrocytes. It is proposed that thisPiinfusion be further evaluated for use as a functional beverage for the prevention and/or treatment of brain injuries and neurodegenerative diseases in which oxidative stress plays a role.

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The antioxidant Rutin counteracts the pathological impact of α-synuclein on the enteric nervous system in vitro

Biological Chemistry ◽

10.1515/hsz-2021-0259 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Anne Christmann ◽

Manuela Gries ◽

Patrik Scholz ◽

Pascal L. Stahr ◽

Jessica Ka Yan Law ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Dopaminergic Neurons ◽

Synaptic Vesicles ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Neuroprotective Effects ◽

The Brain ◽

And Oxidative Stress

Abstract Motoric disturbances in Parkinson’s disease (PD) derive from the loss of dopaminergic neurons in the substantia nigra. Intestinal dysfunctions often appear long before manifestation of neuronal symptoms, suggesting a strong correlation between gut and brain in PD. Oxidative stress is a key player in neurodegeneration causing neuronal cell death. Using natural antioxidative flavonoids like Rutin, might provide intervening strategies to improve PD pathogenesis. To explore the potential effects of micro (mRutin) compared to nano Rutin (nRutin) upon the brain and the gut during PD, its neuroprotective effects were assessed using an in vitro PD model. Our results demonstrated that Rutin inhibited the neurotoxicity induced by A53T α-synuclein (Syn) administration by decreasing oxidized lipids and increasing cell viability in both, mesencephalic and enteric cells. For enteric cells, neurite outgrowth, number of synaptic vesicles, and tyrosine hydroxylase positive cells were significantly reduced when treated with Syn. This could be reversed by the addition of Rutin. nRutin revealed a more pronounced result in all experiments. In conclusion, our study shows that Rutin, especially the nanocrystals, are promising natural compounds to protect neurons from cell death and oxidative stress during PD. Early intake of Rutin may provide a realizable option to prevent or slow PD pathogenesis.

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Lithium Inhibits Oxidative Stress-Induced Neuronal Senescence Through miR-34a

10.21203/rs.3.rs-213621/v1 ◽

2021 ◽

Author(s):

Kemal Ugur Tufekci ◽

Begum Alural ◽

Emre Tarakcioglu ◽

Tugba San ◽

Sermin Genc

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Neurodegenerative Diseases ◽

Cell Cycle Arrest ◽

Neuronal Cells ◽

Neuroprotective Effects ◽

Sudan Black B ◽

Cycle Arrest ◽

Stress Induced Premature Senescence

Abstract Neuronal senescence, triggered by telomere shortening, oncogene activation, DNA damage, or oxidative stress, has been associated with neurodegenerative diseases' pathogenesis. Therefore, preventing neuronal senescence could be a novel treatment strategy for neurodegenerative diseases. Lithium (Li), the first-line treatment against bipolar disorder, has been shown to have neuroprotective effects in clinical, pre-clinical, and in vitro studies. Lithium can protect cells from senescence, and its effect on neuronal senescence was investigated in our study. Furthermore, we also investigated the effects of lithium on the senescence-associated miR-34a/Sirt1/p53 pathway. In this study, hydrogen peroxide was used as an inducer for the "stress-induced premature senescence" model. In the senescence model, we have assessed Li's effects on senescence by analyzing ß-galactosidase activity, Sudan Black B, and senescence-associated heterochromatin foci (SAHF) stainings, and on cell cycle arrest by BrdU staining. Furthermore, expression levels of senescence and cell cycle arrest-related proteins (p53, p21, p16INK4a, and SIRT1) by western blotting. Finally, the effects of Li on senescence-associated miR-34a levels were measured by quantitative PCR. We show via Sudan Black B staining, β-Gal activity assay, and by detecting SAHF, Li protects against senescence in neuronal cells. Then, lithium's effect on signaling has also been determined on pathways involved in senescence and cell cycle arrest. Moreover, we have observed that Li has a modulatory effect on miR-34a expression. Therefore, we posit that Li suppresses senescence in neuronal cells and that this effect is mediated through miR-34a/Sirt1/p53 axis.

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Lovastatin Alleviates α-Synuclein Aggregation and Phosphorylation in Cellular Models of Synucleinopathy

Frontiers in Molecular Neuroscience ◽

10.3389/fnmol.2021.682320 ◽

2021 ◽

Vol 14 ◽

Author(s):

Lijun Dai ◽

Jiannan Wang ◽

Mingyang He ◽

Min Xiong ◽

Ye Tian ◽

...

Keyword(s):

Oxidative Stress ◽

Neurodegenerative Diseases ◽

Lower Risk ◽

Clinical Evidence ◽

Hek293 Cells ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Cellular Models ◽

Potential Value

Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. Pathologically, it is characterized by the aberrant aggregation of α-synuclein (α-syn) in neurons. Clinical evidence shows that patients with hypercholesterolemia are more likely to get PD, while lovastatin users have a lower risk of suffering from it. In this study, we investigated the effects of lovastatin on the aggregation and phosphorylation of α-syn in vitro. Our results demonstrate that α-syn preformed fibrils induce the phosphorylation and aggregation of α-syn in HEK293 cells stably transfected with α-syn-GFP and SH-SY5Y cells as well, which could be attenuated by in a concentration-dependent manner. Besides, lovastatin inhibited oxidative stress, histone acetylation, and the activation of casein kinase 2 (CK2). Collectively, lovastatin alleviates α-syn aggregation and phosphorylation in cellular models of synucleinopathy, indicating its potential value of being adopted in the management of PD.

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Sulforaphane as a Potential Protective Phytochemical against Neurodegenerative Diseases

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/415078 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 137

Author(s):

Andrea Tarozzi ◽

Cristina Angeloni ◽

Marco Malaguti ◽

Fabiana Morroni ◽

Silvana Hrelia ◽

...

Keyword(s):

Neurodegenerative Diseases ◽

Neurological Disorders ◽

Neuronal Loss ◽

In Vivo Studies ◽

Alternative Form ◽

Neuroprotective Effects ◽

Beneficial Effects ◽

Hydrolysis Of

A wide variety of acute and chronic neurodegenerative diseases, including ischemic/traumatic brain injury, Alzheimer’s disease, and Parkinson's disease, share common characteristics such as oxidative stress, misfolded proteins, excitotoxicity, inflammation, and neuronal loss. As no drugs are available to prevent the progression of these neurological disorders, intervention strategies using phytochemicals have been proposed as an alternative form of treatment. Among phytochemicals, isothiocyanate sulforaphane, derived from the hydrolysis of the glucosinolate glucoraphanin mainly present inBrassicavegetables, has demonstrated neuroprotective effects in several in vitro and in vivo studies. In particular, evidence suggests that sulforaphane beneficial effects could be mainly ascribed to its peculiar ability to activate the Nrf2/ARE pathway. Therefore, sulforaphane appears to be a promising compound with neuroprotective properties that may play an important role in preventing neurodegeneration.

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