Kyle J. Norton
Green tea, is a precious drink processes numbers of health benefit known to almost everyone in Asia and Western world.
Neuro degenerative diseases are a class of conditions characterized by deteriorating neurons and accumulated plaque in blocking the neuro transmitters of the brain and spinal cords in performance of normal functions.
Epidemiological studies strongly suggested that green tea and its bioactive chemical constituents, particularly, Epigallocatechin-3-gallate (EGCG) may have potential and therapeutic implications in reduced early onset, progreeion and treatment of Neuro Degenerative Diseases However, geographic differences where the tea are growth, types of tea, time of harvest, time of feeding, how the tea are fermented,.....may effect the quality of tea in prevention of tumor onset.
The differentiation of green tea bioactive constituents in risk of neuro-degenerative diseases was found to associate to numbers of mechanism through many different aspects(1).
According to the statistic, approximately, 5 million Americans suffer from Alzheimer's disease, 1 million from Parkinson's and 400,000 from multiple sclerosis (MS) today, inducing overwhelming social, economic and health care burden on society.
The differentiation of green tea bioactive constituents in risk of neuro-degenerative diseases was found to associate to numbers of mechanism through many different aspects(1).
According to the statistic, approximately, 5 million Americans suffer from Alzheimer's disease, 1 million from Parkinson's and 400,000 from multiple sclerosis (MS) today, inducing overwhelming social, economic and health care burden on society.
The investigation of green tea bioactive epigallocatechin-gallate (EGCG) activities in lipopolysaccharide- (LPS-) mediated systemic inflammation in induction of neurodegenerative diseases suggested that application of green tea chemical constituent demonstrated a significant effect in ameliorated LPS induced expression of proinflammatory cytokines of tumor necrosis factor alphaTNF-α(2), a cell signalling protein involved in systemic inflammation in the acute phase of infection, and interleukin 1 beta (IL1β)(2), an cytokine with function in the regulation of immune and inflammatory responses to infections or sterile insults and interleukin 6 (IL-6)(2) involved in inflammation and infection responses, particularly, in the inhibition of the expressions of inflammatory cytokines in the mononuclear blood cells (PBMCs), consisting lymphocytes (T cells, B cells, NK cells) with function to clear away of debris in the infection site.
The activation of inflammatory cytokines expression caused by lipopolysaccharide- (LPS) injection can trigger neurotoxicity(2), leading to neurons brains progressive degeneration, resulting in elevated risk of neuro degenerative diseases.
Application of green tea bioactive epigallocatechin-gallate (EGCG) was found not only inhibited LPS(2) in precipitation of toxicity in resolved inflammation and mediated neuroprotection but also exerted anti toxicity(2) through its antioxidant activity in decreased expression of reactive oxygen species in triggered brain cell apoptosis.
Interleukin 6 (IL-6) acts as both pro-inflammatory cytokines and an anti-inflammatory mytokines with function involved inflammation responses at sites of acute and chronic infection.
Green tea Epigallo-catechin-3-gallate (EGCG) in the aspect of ROS in risk of neuro-degeneration in the dentate gyrus, part of the hippocampus and/or hippocampal formation of C57Bl/6 mice, suggested that the application promoted neural precursor cell(3), (a partially differentiated cell) proliferation, without changes at the level of immature and mature new neurons(3).
In adult hippocampal neurogenesis in male Balb/C mice, injection of green tea bioactive compounds in different doses also expressed a strong implication of increased cells survival without affecting cell proliferation but decreasing apoptotic cells(3).
The increased production of neuro precursor cell in stimulated neuro generation and increased cell survival from green tea was attributed to the green tea antioxidants acted as free radical scavengers to ameliorate chain reaction stimulated by reactive oxygen species (ROS)(2)(3).
Green tea treatment was found to promote production of more elaborated dendritic (structures on the neuron that receive electrical messages) trees(3) in young DCX-positive neurons with function in acquisition of spatial learning, as well as reversal learning, but not the retrieval of stored long-term memories.
Implication of green tea bio compounds EGCG also significantly increased net growth and development of nervous tissue in the adult hippocampus(3) and hippocampal levels of phospho-Akt(3).in regulated multiple cellular processes, including glucose metabolism, apoptosis, cell proliferation, transcription and cell migration by re-establishing the function of PI3K(3) in intracellular signaling pathway.
Dr. Neha Atulkumar Singh(3), the lead author in the article of "Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG)",said, "there is a need to identify a class of drug capable of reversing neural damage and preventing further neural death" and "assesses the reliability of the neuroprotective benefits of epigallocatechin-gallate (EGCG) by shedding light on their biological, pharmacological, antioxidant and metal chelation properties, with emphasis on their ability to invoke a range of cellular mechanisms in the brain".
The activation of inflammatory cytokines expression caused by lipopolysaccharide- (LPS) injection can trigger neurotoxicity(2), leading to neurons brains progressive degeneration, resulting in elevated risk of neuro degenerative diseases.
Application of green tea bioactive epigallocatechin-gallate (EGCG) was found not only inhibited LPS(2) in precipitation of toxicity in resolved inflammation and mediated neuroprotection but also exerted anti toxicity(2) through its antioxidant activity in decreased expression of reactive oxygen species in triggered brain cell apoptosis.
Interleukin 6 (IL-6) acts as both pro-inflammatory cytokines and an anti-inflammatory mytokines with function involved inflammation responses at sites of acute and chronic infection.
Green tea Epigallo-catechin-3-gallate (EGCG) in the aspect of ROS in risk of neuro-degeneration in the dentate gyrus, part of the hippocampus and/or hippocampal formation of C57Bl/6 mice, suggested that the application promoted neural precursor cell(3), (a partially differentiated cell) proliferation, without changes at the level of immature and mature new neurons(3).
In adult hippocampal neurogenesis in male Balb/C mice, injection of green tea bioactive compounds in different doses also expressed a strong implication of increased cells survival without affecting cell proliferation but decreasing apoptotic cells(3).
The increased production of neuro precursor cell in stimulated neuro generation and increased cell survival from green tea was attributed to the green tea antioxidants acted as free radical scavengers to ameliorate chain reaction stimulated by reactive oxygen species (ROS)(2)(3).
Green tea treatment was found to promote production of more elaborated dendritic (structures on the neuron that receive electrical messages) trees(3) in young DCX-positive neurons with function in acquisition of spatial learning, as well as reversal learning, but not the retrieval of stored long-term memories.
Implication of green tea bio compounds EGCG also significantly increased net growth and development of nervous tissue in the adult hippocampus(3) and hippocampal levels of phospho-Akt(3).in regulated multiple cellular processes, including glucose metabolism, apoptosis, cell proliferation, transcription and cell migration by re-establishing the function of PI3K(3) in intracellular signaling pathway.
Dr. Neha Atulkumar Singh(3), the lead author in the article of "Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG)",said, "there is a need to identify a class of drug capable of reversing neural damage and preventing further neural death" and "assesses the reliability of the neuroprotective benefits of epigallocatechin-gallate (EGCG) by shedding light on their biological, pharmacological, antioxidant and metal chelation properties, with emphasis on their ability to invoke a range of cellular mechanisms in the brain".
1. Dementia
Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age.
In the 5.7-year prospective cohort study, using a questionnaire, information on daily green tea consumption and other lifestyle factors collected from elderly Japanese individuals aged 65 years or more, green tea consumption is associated to reduced risk of dementia with a incidence of occurrence rate of 8.7%(4).
Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age.
In the 5.7-year prospective cohort study, using a questionnaire, information on daily green tea consumption and other lifestyle factors collected from elderly Japanese individuals aged 65 years or more, green tea consumption is associated to reduced risk of dementia with a incidence of occurrence rate of 8.7%(4).
In the intracerebroventricular (ICV) infusion of streptozotocin (STZ) animal model explicit chronic brain dysfunction involved long-term and progressive deficits in learning, memory, and cognitive behavior, along with a permanent and ongoing cerebral energy deficit, mice treated with green tea EGCG at a dose of 10mg/kg/day for 4 weeks, showed a significant improvement in reduced oxidative stress parameter against production of inflammatory and free radical expression(5).
These inhibitions can be seen in the diminished AChE(5), glutathione peroxidase activity(5) as well as NO metabolites(5), and reactive oxygen species contents(5).
The enhanced antioxidants status induced neuroprotective effect is result of EGCG injection in ameliorated inflammatory and free radical causes of cell death in brain of treated mice.
Dr. Tomata Y(5), the lead author of the study said, "The lower risk of incident dementia was consistent even after selecting participants who did not have subjective memory complaints at the baseline."
More explicitly, in the finding of a natural food for reverse or delay of risk factors of dementia and AD, vascular, metabolic, and lifestyle-related factors involved development of dementia and late-life cognitive disorders, green tea with high amount of caffeine stimulate the psychoactive effects in attenuated cognitive impairment/decline and dementia(6) through heightened alertness and arousal and improvement of cognitive performance.
Such results have been proposed by several cross-sectional and longitudinal population-based studies, particular in patients with mild cognitive impairment and progression to dementia(6).
2. Alzheimer's disease
Alzheimer's disease is a neuro-degenerative condition of loss or decrease of cognitive and memory functions due to aging.
According to the Maternal and Infant Health, ASL NA 3 SUD, epigallocatechin and gallic acid, (-)-Epigallocatechin-3-Gallate (EGCG), found in green tea exerted a strong anti-inflammatory and anti oxidative properties in protection against neuronal damage(7) and brain edema(7).
The study also stated that green tea may also contribute to reduced risk and treatment of AD by ameliorated chronic viral infection(7), one of the cause in responsible for AD's neuropathology.
Dr. Mandel SA(7). the lead author and expert in green tea study said, "tea drinking may decrease the incidence of dementia, AD, and PD. In particular, its main catechin polyphenol constituent (-)-epigallocatechin-3-gallate (EGCG) has been shown to exert neuroprotective/neurorescue activities in a wide array of cellular and animal models of neurological disorders".
Other researchers suggested that the efficacy of epigallocatechin and gallic acid, (-)-Epigallocatechin-3-Gallate (EGCG) in reduced risk of AD may be attributed to the antioxidant activity in ameliorated production of ROS in induced risk of oxidative stress(8) which has been found to associate to production of lipid peroxidation, leading to abnormal deposition of amyloid β (Aβ) peptide(8) and free radical over expression in aging people also vulnerable to imbalance of antioxidant and ROS
may have a negatively direct interaction with proteins, nucleic acids, and other molecules and may also alter their structures and functions in inducing risk AD.
In a animal study to evaluate the efficacy of Caffeic acid(9) in AD, mice rats randomly divided into three groups: i) control group, ii) AD model group and iii) caffeic acid group, mice fed with the phytochemical expressed a significant in increased learning deficit and cognitive function(9) demonstrated by the Morris water maze task in compared control.
Additionally, fed mice also displayed of attenuated oxidative stress(9), inflammation, nuclear factor‑κB‑p65 protein expression(9) involved inflammatory cytokins production and suppressed caspase‑3 activity induced cell death and other mechanisms in the rats with AD.
Inflammatory process has shown to have an negative role in increased risk of AD, by causing neuroinflammation(10), including brain cells such as microglia and astrocytes and subsequently in promoted dysfunction and neuronal death(10). Therefore by suppressing production of inflammatory cytokins, caffeic acid expressed a significant reduction of AD risk.
The efficacy in contribution of cognitive improvement following caffeic acid application may be due to its antioxidant activity and restoration of cholinergic functions(10), as deficiency of cholinergic function has shown to effect cognition, behavior and activities of daily living.
3. Parkinson's disease (PD)
Parkinson's disease (PD) is a progressive neurodegenerative disease, causing severe depletion of glutamatergic and dopaminergic inputs in the striatum.
Application of metal chelation was found to ameliorated the expression of ROS in induction of oxidative stress(11) through a chain of reaction and precipitation of aggregation of alpha-synuclein and beta-amyloid peptides deposit in the brain, main leading causes to the onset of PD.
In iron abnormality PD subjects, oxidopamine, also known as 6-hydroxydopamine or 2,4,5-trihydroxyphenethylamine(6-OHD), a neurotoxic synthetic organic compound was found to disrupt iron metabolism(12), leading to over expression of the iron induction of dyshomeostasis cause of iron toxicity and oxidative damage in dopaminergic neurons.
Green tea major polyphenol, (−)-epigallocatechin-3-gallate used in metal chelation, ameliorated iron dependent free radicals located in the subcellular compartments and cellular membranes(12), through the effect in inhibited iron input and exhibited iron output in brain areas where it preferentially accumulates in neurodegenerative diseases, particularly Parkinsons' disease.
The neurotoxin 6-OHDA causes of iron unstable equilibrium, green extract GECG administration improved the function of hepcidin(12), a liver-derived hormone in regulated iron dyshomeostasis and gene expression of the iron metabolism through expressions of iron regulatory proteins (IRP1 and IRP2) in regulated the RNA level, between the transcription and the translation of the gene in expression of the iron homeostasis.
In the differentiation of neurotoxin 6-OHDA induced iron dyshomeostasis in increased oxidative stress in damage to neuron cells(12), green extract GECG effects demonstrated a significant inhibition of free radical and iron free radical expression in the cellular membranes(12) through the antioxidant activities and anti-inflammatory system and expression of nuclear factor-like 2(Nrf2)(12) in stimulated production of antioxidant in protection against oxidative damage during injury and inflammation; heme oxygenase-1(HO-1)(12) in increased production of superoxide dismutase and catalase against ROS and peroxisome proliferator-activated receptor gamma (PPARγ)(12) in regulated production of pro and anti inflammatory cytokines and mytokines..
By reducing the over expression of oxidative damage to neuron cells through regulation of iron related factors as mentioned above, iron chelator EGCG can counteract these adverse effects and prevent onset of PD.
Parkinson's disease (PD) is a progressive neurodegenerative disease, causing severe depletion of glutamatergic and dopaminergic inputs in the striatum.
Application of metal chelation was found to ameliorated the expression of ROS in induction of oxidative stress(11) through a chain of reaction and precipitation of aggregation of alpha-synuclein and beta-amyloid peptides deposit in the brain, main leading causes to the onset of PD.
In iron abnormality PD subjects, oxidopamine, also known as 6-hydroxydopamine or 2,4,5-trihydroxyphenethylamine(6-OHD), a neurotoxic synthetic organic compound was found to disrupt iron metabolism(12), leading to over expression of the iron induction of dyshomeostasis cause of iron toxicity and oxidative damage in dopaminergic neurons.
Green tea major polyphenol, (−)-epigallocatechin-3-gallate used in metal chelation, ameliorated iron dependent free radicals located in the subcellular compartments and cellular membranes(12), through the effect in inhibited iron input and exhibited iron output in brain areas where it preferentially accumulates in neurodegenerative diseases, particularly Parkinsons' disease.
The neurotoxin 6-OHDA causes of iron unstable equilibrium, green extract GECG administration improved the function of hepcidin(12), a liver-derived hormone in regulated iron dyshomeostasis and gene expression of the iron metabolism through expressions of iron regulatory proteins (IRP1 and IRP2) in regulated the RNA level, between the transcription and the translation of the gene in expression of the iron homeostasis.
In the differentiation of neurotoxin 6-OHDA induced iron dyshomeostasis in increased oxidative stress in damage to neuron cells(12), green extract GECG effects demonstrated a significant inhibition of free radical and iron free radical expression in the cellular membranes(12) through the antioxidant activities and anti-inflammatory system and expression of nuclear factor-like 2(Nrf2)(12) in stimulated production of antioxidant in protection against oxidative damage during injury and inflammation; heme oxygenase-1(HO-1)(12) in increased production of superoxide dismutase and catalase against ROS and peroxisome proliferator-activated receptor gamma (PPARγ)(12) in regulated production of pro and anti inflammatory cytokines and mytokines..
By reducing the over expression of oxidative damage to neuron cells through regulation of iron related factors as mentioned above, iron chelator EGCG can counteract these adverse effects and prevent onset of PD.
The mechanism on disruption of iron metabolism by 6-OHDA in PD cell line N27, discovered that application of the iron chelator EGCG also disrupts the iron dyshomeostasis in N27 cells(12) (dopaminergic neural cell line) induced by 6-OHDA through regulating iron transporters and regulators expression, such as DMT1(12) with function in mediation of the entry of dietary iron into these mucosal cells and TfR(12), a carrier protein for transferrin with function in import iron into the cell and regulated response to intracellular iron concentration and hepcidin, a central regulator in maintain iron homeostasis.
Dysregulation of hepcidin production results in a variety of iron disorders.
In 6-OHDA induced neurotoxicity to cause PD, administration of green tea GECG also reduced the intracellular iron retention(12) by decreasing the iron importers and increasing iron exporters, through regulation of the function of iron-regulated transporters, such as ferroportin.
There was a report suggested that intervention of 3 cups of green tea daily for 3 months improved the antioxidant status and reduced oxidative damage in early PD patients without affecting their iron status.
4. Cognitive impairment
Cognitive impairment is a condition of decline of memory and thinking skills due to aging considered as an early sign of neuro degenerative diseases.In a total of 12 elderly nursing home residents with cognitive dysfunction, participants who drink green tea powder 2 g/day for 3 months showed a significantly improved cognitive performance(13) and reduced the progression of cognitive dysfunction(13) indicated by Mini-Mental State Examination Japanese version (MMSE-J) score.
Other study (Japanese residents aged >60 years from Nakajima, Japan (the Nakajima Project) of 723 participants with normal cognitive function at a baseline survey (2007-2008), the 490 completed the follow up survey in 2011-2013, suggested that incidence of dementia and cognitive impairment are lower(14) among individuals who consumed green tea 1-6 days per week compared with individuals who did not consume green tea at all(14).
According to the double-blind, randomized controlled study of 39 nursing home residents with cognitive dysfunction (four men, 29 women) divided into two group either with
consumption of 2 g/day of green tea powder (containing 220.2 mg of catechins) or placebo powder (containing 0.0 mg of catechins), green tea treated group showed a significantly reduced cognitive dysfunction(15) in 3 months follow up in compared to placebo.
The efficacy of green tea in decreased progression of cognitive impairment in the short term may be attributed to ameliorated oxidative stress and levels of low-density lipoprotein.
Memory deficit are medical condition characterized lost of the ability in store and recall past information, such as knowledge, sensation, thoughts,......
Lost of memory function is not only associated with normal aging progression in adult population but considered as a feature of neurodegenerative diseases, including psychiatric and neurological disorders.
According to the Harvard neuro discovery center, today, approximately 5 million Americans suffer from Alzheimer's disease; 1 million from Parkinson's; 400,000 from multiple sclerosis (MS); 30,000 from amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), and 30,000 from Huntington's disease.
The evaluate green tea extract (GTex) and its major functional polyphenol (−)-epigallocatechin gallate (EGCG) effect on memory of cerebral ischemic rats showed that green tea EGCG and pentoxifylline (PTX), a methylxanthine derivative with anti-inflammatory function, application after 1 hour demonstrates a strong efficacy in improved ishemic-induced memory impairment(16), according to Morris water maze test.
Long term treatment of green tea EGCG also displayed a significant increase level of antioxidant such as malondialdehyde (MDA) levels(16), glutathione (GSH)(16), and superoxide dismutase (SOD)(16) activity in the cerebral cortex and hippocampus, through prevented cerebral infraction breakdown of MDA and GSH in the hippocampus(16), in protected against damage to cellular components caused by reactive oxygen species (ROS) including free radicals, peroxides, lipid peroxides....
Green tea EGCG inhibited BV-2 microglia cells in induction of brain inflammatory effect(16) in precipitated neurodegeneration and neuro toxicology to facilitate memory impairment, through ameliorated the expression of lipopolysaccharide- (LPS-)(16) in exhibited free radical nitric oxide production which are associated to in initiated neurotoxicity.
The application also ameliorated the cyclooxygenase-2 (COX-2) expression(17) associated with pro-inflammatory activities in mediated neurodegenerative processes of several acute and chronic diseases and expression of the inducible nitric oxide synthase (iNOS)(17), one of the direct consequences of an inflammatory process in the BV-2 cells.
The experiment of cerebral ischemia animal model indicated that green extract and its active polyphenol EGCG improved learning and memory deficits through exhibited antioxidant activity(17) in reduction of oxidative stress and neuro-inflammation.
Moreover, green tea Epigallocatechin gallate (EGCG) with beneficial effects on the impairment in learning and memory also demonstrated in increased autophagic activation in getting rid of damage and dysfunctional cell accumulation(17) to protect healthy neuron from stressful conditions, such as over expression of ROS presentation, according to the experiment of chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and observed through the elevated LC3-II, a reliable method for monitoring autophagy and autophagy-related processes, including autophagic cell death.and p62 protein level, an useful marker for the induction of autophagy(17),
At the same time, the green tea EGCG also displayed a strong inhibition of increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling(17) caused by implication of chronic unpredictable mild stress (CUMS) in the CA1 regions in the hippocampal circuit*17) in initiation of the pathophysiology of memory deficits, thus reducing amyloid beta1-42 (Aβ1-42) deposit, and restored autophagic degradation activity(17).
Mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling pathway is an essential cellular signaling pathway involved a number of important physiological functions, including cell growth, proliferation, metabolism, protein synthesis, and autophagy.
The information finding suggested that green tea with abundant bioactive polyphenols, such as (-)-Epigallocatechin-3-Gallate (EGCG may be considered as a function foods for reduced risk and used combination with standard medicine for treatment of Neuro Degenerative Diseases
However,intake of single ingredient isolated from green tea, epigallocatechin and gallic acid, (-)-Epigallocatechin-3-Gallate (EGCG) have been found to cause toxicity(18)(19) in some cases in medical literature. Therefor, long term take of green extract should be taken with extreme care.
6. Inhibited β-amyloid
β-amyloid are plaques found in the brains of Alzheimer patients derived from the amyloid precursor protein (APP) with function in binding to other proteins on the surface of cells.
The differentiation of green tea activities in risk of plagues deposit in certain parts of the brain to induce development and neuropathogenesis of dementia was found to associate to numbers of implication through several mechanisms.
In the study to clarify the effect of green tea Epigallocatechin-3-gallate (EGCG) in inhibited activities of nitrosative as well as oxidative stress in induction of Abeta-cause of damages in neurons and glial cells surround neurons, researchers at the Daegu Haany University found that application of the phytophenols exerts a significant interference in ameliorated the elevation of Abeta-induced by oxidative and/or nitrosative to facilitate cell death through its antioxidant and anti-inflammatory properties(20).
Further analysis found that green tea bioactive compound reduced activities of Abeta injection in induction of nitrosative stress on BV2 cells caused by increased expression of inducible nitric oxide synthase (iNOS) in production of nitric oxide (NO) and peroxynitrite(20), in elevated cytotoxicity to precipitate apoptosis, though inhibited reactive nitrogen species act together with reactive oxygen species to establish chain reaction in damage to BV2 cells(20).
In cellular metabolism, pretreatment of green tea EGCG also demonstrated a strong antioxidant properties in induction of neuroprotective effect by fortified cellular GSH over expression through elevated mRNA expression of galuatehe eva-glutamylcysteine ligase (GCL)(20) with functions involved production of cellular antioxidant glutathione (GSH).
Additionally, the examine the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Abeta(1-42) with oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Abeta(1-42) (2 microg/mouse, icv), suggested that green tea bioactive l-theanine component exerts a significantly attenuated Abeta(1-42) levels induced memory impairment by precipitated neuronal cell death in the cortex and hippocampus of the brain(21).
Moreover, l-theanine also inhibited Abeta(1-42)-induced extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase and activity of nuclear factor kappaB (NF-kappaB) in initiated cellular apoptosis caused by reactive nitrogen species hyper activities(21).
Further more, the bioactive l-theanine also significantly reduced oxidative protein and lipid damage and elevated glutathione levels in the brain, thus reducing macromolecular oxidative damage in improved memory.
Additional study of green tea effect in attenuated accumulation of β-amyloid (Aβ) peptide plaques is a major pathogenic event in Alzheimer's disease (AD) opinionated that in the wild type amyloid precursor protein (APP) transfected (N2a/APP695) cell line, Epigallocatechin gallate (EGCG), a highly active catechin found in green tea, significantly reinforce the activity of nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), a regulator of adipocyte differentiation by promoting its mRNA and protein expressions in N2a/APP695 cells, thus attenuated Aβ generation in N2a/APP695 cells in induction of Alzheimer's disease (AD)(22).
Intriguingly, the efficacy of Epigallocatechin gallate (EGCG) in inhibited β-amyloid (Aβ) peptide plaques accumulation was found to be attributed by its antioxidant activity in decreased the expression of pro-apoptotic proteins (Bax, caspase-3) activated by Aβ insults, the activity of the anti-inflammatory agent NF-κB triggered by β-amyloid (Aβ) peptide and inhibited the oxidative stress by decreasing the levels of ROS and MDA and increased the expression of antioxidant enzyme MnSOD(23).
7. Amyotrophic Lateral Fclerosis (Lou Gehrig's disease)
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a specific disease involved the death of neurons in controlling voluntary muscles.
According to the research published by the Hanyang University, administration of green tea Epigallocatechin gallate (EGCG) exerted a neuroprotective effect in reduced oxidative stress in orchestrated death of neurons(24).
In the evaluation of green tea EGCG in risk of amyotrophic lateral sclerosis (ALS) in human G93A(with function in responsible for destroying free superoxide radicals in the body) mutated Cu/Zn-superoxide dismutase (SOD1) gene in mice model, scientists found that application of green tea EGCG at doses of 1.5, 2.9, and 5.8 microg/g body weight, dissolved in 0.5 ml of 0.9% sterile NaCl intraorally every day after 60 days of age demonstrate significant effects in prolonged the symptom onset and life span of ALS mice through preserved more survival and attenuated death signals(24).
The result of increased life span of mutated gene mice was attributed to increased antioxidant activity of green tea in inhibited the levels of ROS in reduced cytotoxicity in initiated death of neurons in controlling voluntary muscles(24).
Further analysis of the effect of green tea in mutated SOD1-G93A in transgenic mice and wild-type mice randomly divided into EGCG-treated groups (10 mg/kg, p.o) and vehicle-treated control groups to assess the motor function, starting at the age of 70 days researchers found that injection of green tea treatment mice display a strong effect in delayed the onset of disease, and extended life span, similar to those in the Hanyang study(24).
Additional differentiation also indicated that green tea treatment group stimulated the production of numbers of new motor neurons in compared to control mice,
Interestingly, the application also decreased the over expression of microglial activation in initiated the inflammatory response due to neuronal damage and removed the damaged cells caused by phagocytosis production(25).
Prolonged and over expression of inflammatory cytokines may increase risk of neuron damage and in some cases death of the nerve cells(25).
Researchers in depth analysis showed that green tea reduced immunohistochemical reaction of NF-kappaB in response to the neuron damage (by antigens) through stimulated production of pro inflammatory factors (as antibody) and cleaved caspase-3 in induction of neuron apoptosis(25).
Moreover, application of green EGCG also expressed a similar result as in other studies in decreased protein level of iNOS and NF-kappaB in the spinal cords in orchestrated free radical NO levels and inflammatory cytokines in neuron cell death in the spinal cord involving the onset of ALS(25).
Dr. Xu Z, the lead author after taking into account of other co founders said, "this study provides further evidences that EGCG has multifunctional therapeutic effects in the mouse model of ALS".
These result were supported by the study of the green tea effect in risk of Lou Gehrig's disease through reviewing the food selection of 44-item food frequency questionnaire of 1 million men and women enrolled and conducted in 1989 through 2002 for ALS mortality(26).
According to results of the study, researchers at the Harvard School of Public Health suggested that green tea injection is associated to reduced mortality rate of patients.
Lost of memory function is not only associated with normal aging progression in adult population but considered as a feature of neurodegenerative diseases, including psychiatric and neurological disorders.
According to the Harvard neuro discovery center, today, approximately 5 million Americans suffer from Alzheimer's disease; 1 million from Parkinson's; 400,000 from multiple sclerosis (MS); 30,000 from amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), and 30,000 from Huntington's disease.
The evaluate green tea extract (GTex) and its major functional polyphenol (−)-epigallocatechin gallate (EGCG) effect on memory of cerebral ischemic rats showed that green tea EGCG and pentoxifylline (PTX), a methylxanthine derivative with anti-inflammatory function, application after 1 hour demonstrates a strong efficacy in improved ishemic-induced memory impairment(16), according to Morris water maze test.
Long term treatment of green tea EGCG also displayed a significant increase level of antioxidant such as malondialdehyde (MDA) levels(16), glutathione (GSH)(16), and superoxide dismutase (SOD)(16) activity in the cerebral cortex and hippocampus, through prevented cerebral infraction breakdown of MDA and GSH in the hippocampus(16), in protected against damage to cellular components caused by reactive oxygen species (ROS) including free radicals, peroxides, lipid peroxides....
Green tea EGCG inhibited BV-2 microglia cells in induction of brain inflammatory effect(16) in precipitated neurodegeneration and neuro toxicology to facilitate memory impairment, through ameliorated the expression of lipopolysaccharide- (LPS-)(16) in exhibited free radical nitric oxide production which are associated to in initiated neurotoxicity.
The application also ameliorated the cyclooxygenase-2 (COX-2) expression(17) associated with pro-inflammatory activities in mediated neurodegenerative processes of several acute and chronic diseases and expression of the inducible nitric oxide synthase (iNOS)(17), one of the direct consequences of an inflammatory process in the BV-2 cells.
The experiment of cerebral ischemia animal model indicated that green extract and its active polyphenol EGCG improved learning and memory deficits through exhibited antioxidant activity(17) in reduction of oxidative stress and neuro-inflammation.
Moreover, green tea Epigallocatechin gallate (EGCG) with beneficial effects on the impairment in learning and memory also demonstrated in increased autophagic activation in getting rid of damage and dysfunctional cell accumulation(17) to protect healthy neuron from stressful conditions, such as over expression of ROS presentation, according to the experiment of chronic unpredictable mild stress (CUMS)-induced cognitive impairment in rats and observed through the elevated LC3-II, a reliable method for monitoring autophagy and autophagy-related processes, including autophagic cell death.and p62 protein level, an useful marker for the induction of autophagy(17),
At the same time, the green tea EGCG also displayed a strong inhibition of increased neuronal loss and activated mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling(17) caused by implication of chronic unpredictable mild stress (CUMS) in the CA1 regions in the hippocampal circuit*17) in initiation of the pathophysiology of memory deficits, thus reducing amyloid beta1-42 (Aβ1-42) deposit, and restored autophagic degradation activity(17).
Mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6k) signaling pathway is an essential cellular signaling pathway involved a number of important physiological functions, including cell growth, proliferation, metabolism, protein synthesis, and autophagy.
The information finding suggested that green tea with abundant bioactive polyphenols, such as (-)-Epigallocatechin-3-Gallate (EGCG may be considered as a function foods for reduced risk and used combination with standard medicine for treatment of Neuro Degenerative Diseases
However,intake of single ingredient isolated from green tea, epigallocatechin and gallic acid, (-)-Epigallocatechin-3-Gallate (EGCG) have been found to cause toxicity(18)(19) in some cases in medical literature. Therefor, long term take of green extract should be taken with extreme care.
6. Inhibited β-amyloid
β-amyloid are plaques found in the brains of Alzheimer patients derived from the amyloid precursor protein (APP) with function in binding to other proteins on the surface of cells.
The differentiation of green tea activities in risk of plagues deposit in certain parts of the brain to induce development and neuropathogenesis of dementia was found to associate to numbers of implication through several mechanisms.
In the study to clarify the effect of green tea Epigallocatechin-3-gallate (EGCG) in inhibited activities of nitrosative as well as oxidative stress in induction of Abeta-cause of damages in neurons and glial cells surround neurons, researchers at the Daegu Haany University found that application of the phytophenols exerts a significant interference in ameliorated the elevation of Abeta-induced by oxidative and/or nitrosative to facilitate cell death through its antioxidant and anti-inflammatory properties(20).
Further analysis found that green tea bioactive compound reduced activities of Abeta injection in induction of nitrosative stress on BV2 cells caused by increased expression of inducible nitric oxide synthase (iNOS) in production of nitric oxide (NO) and peroxynitrite(20), in elevated cytotoxicity to precipitate apoptosis, though inhibited reactive nitrogen species act together with reactive oxygen species to establish chain reaction in damage to BV2 cells(20).
In cellular metabolism, pretreatment of green tea EGCG also demonstrated a strong antioxidant properties in induction of neuroprotective effect by fortified cellular GSH over expression through elevated mRNA expression of galuatehe eva-glutamylcysteine ligase (GCL)(20) with functions involved production of cellular antioxidant glutathione (GSH).
Additionally, the examine the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Abeta(1-42) with oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Abeta(1-42) (2 microg/mouse, icv), suggested that green tea bioactive l-theanine component exerts a significantly attenuated Abeta(1-42) levels induced memory impairment by precipitated neuronal cell death in the cortex and hippocampus of the brain(21).
Moreover, l-theanine also inhibited Abeta(1-42)-induced extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase and activity of nuclear factor kappaB (NF-kappaB) in initiated cellular apoptosis caused by reactive nitrogen species hyper activities(21).
Further more, the bioactive l-theanine also significantly reduced oxidative protein and lipid damage and elevated glutathione levels in the brain, thus reducing macromolecular oxidative damage in improved memory.
Additional study of green tea effect in attenuated accumulation of β-amyloid (Aβ) peptide plaques is a major pathogenic event in Alzheimer's disease (AD) opinionated that in the wild type amyloid precursor protein (APP) transfected (N2a/APP695) cell line, Epigallocatechin gallate (EGCG), a highly active catechin found in green tea, significantly reinforce the activity of nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), a regulator of adipocyte differentiation by promoting its mRNA and protein expressions in N2a/APP695 cells, thus attenuated Aβ generation in N2a/APP695 cells in induction of Alzheimer's disease (AD)(22).
Intriguingly, the efficacy of Epigallocatechin gallate (EGCG) in inhibited β-amyloid (Aβ) peptide plaques accumulation was found to be attributed by its antioxidant activity in decreased the expression of pro-apoptotic proteins (Bax, caspase-3) activated by Aβ insults, the activity of the anti-inflammatory agent NF-κB triggered by β-amyloid (Aβ) peptide and inhibited the oxidative stress by decreasing the levels of ROS and MDA and increased the expression of antioxidant enzyme MnSOD(23).
7. Amyotrophic Lateral Fclerosis (Lou Gehrig's disease)
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a specific disease involved the death of neurons in controlling voluntary muscles.
According to the research published by the Hanyang University, administration of green tea Epigallocatechin gallate (EGCG) exerted a neuroprotective effect in reduced oxidative stress in orchestrated death of neurons(24).
In the evaluation of green tea EGCG in risk of amyotrophic lateral sclerosis (ALS) in human G93A(with function in responsible for destroying free superoxide radicals in the body) mutated Cu/Zn-superoxide dismutase (SOD1) gene in mice model, scientists found that application of green tea EGCG at doses of 1.5, 2.9, and 5.8 microg/g body weight, dissolved in 0.5 ml of 0.9% sterile NaCl intraorally every day after 60 days of age demonstrate significant effects in prolonged the symptom onset and life span of ALS mice through preserved more survival and attenuated death signals(24).
The result of increased life span of mutated gene mice was attributed to increased antioxidant activity of green tea in inhibited the levels of ROS in reduced cytotoxicity in initiated death of neurons in controlling voluntary muscles(24).
Further analysis of the effect of green tea in mutated SOD1-G93A in transgenic mice and wild-type mice randomly divided into EGCG-treated groups (10 mg/kg, p.o) and vehicle-treated control groups to assess the motor function, starting at the age of 70 days researchers found that injection of green tea treatment mice display a strong effect in delayed the onset of disease, and extended life span, similar to those in the Hanyang study(24).
Additional differentiation also indicated that green tea treatment group stimulated the production of numbers of new motor neurons in compared to control mice,
Interestingly, the application also decreased the over expression of microglial activation in initiated the inflammatory response due to neuronal damage and removed the damaged cells caused by phagocytosis production(25).
Prolonged and over expression of inflammatory cytokines may increase risk of neuron damage and in some cases death of the nerve cells(25).
Researchers in depth analysis showed that green tea reduced immunohistochemical reaction of NF-kappaB in response to the neuron damage (by antigens) through stimulated production of pro inflammatory factors (as antibody) and cleaved caspase-3 in induction of neuron apoptosis(25).
Moreover, application of green EGCG also expressed a similar result as in other studies in decreased protein level of iNOS and NF-kappaB in the spinal cords in orchestrated free radical NO levels and inflammatory cytokines in neuron cell death in the spinal cord involving the onset of ALS(25).
Dr. Xu Z, the lead author after taking into account of other co founders said, "this study provides further evidences that EGCG has multifunctional therapeutic effects in the mouse model of ALS".
These result were supported by the study of the green tea effect in risk of Lou Gehrig's disease through reviewing the food selection of 44-item food frequency questionnaire of 1 million men and women enrolled and conducted in 1989 through 2002 for ALS mortality(26).
According to results of the study, researchers at the Harvard School of Public Health suggested that green tea injection is associated to reduced mortality rate of patients.
The information finding suggested that green tea with abundant bioactive polyphenols, such as (-)-Epigallocatechin-3-Gallate (EGCG may be considered as a function foods for reduced risk and used combination with standard medicine for treatment of Neuro Degenerative Diseases
However,intake of single ingredient isolated from green tea, epigallocatechin and gallic acid, (-)-Epigallocatechin-3-Gallate (EGCG) have been found to cause toxicity(18)(19) in some cases in medical literature. Therefor, long term take of green extract should be taken with extreme care.
For More information of yoga lessons tailor to a complete well being for women, please visit: YOGA FOR WOMEN
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.
However,intake of single ingredient isolated from green tea, epigallocatechin and gallic acid, (-)-Epigallocatechin-3-Gallate (EGCG) have been found to cause toxicity(18)(19) in some cases in medical literature. Therefor, long term take of green extract should be taken with extreme care.
For More information of yoga lessons tailor to a complete well being for women, please visit: YOGA FOR WOMEN
Arthritis Is Curable
You Can Eliminate Osteoarthritis
By addressing the Underlying Causes through Clinical Trials and Studies
Ovarian Cysts And PCOS Elimination
Holistic System In Existence That Will Show You How To
Permanently Eliminate All Types of Ovarian Cysts Within 2 Months
FOOD HACK for Weight Loss
A Simple Cooking Technique That Cuts The Calories & Glycemic
Impact In Rice, Pasta, And Potatoes In Half
You Can Eliminate Osteoarthritis
By addressing the Underlying Causes through Clinical Trials and Studies
Ovarian Cysts And PCOS Elimination
Holistic System In Existence That Will Show You How To
Permanently Eliminate All Types of Ovarian Cysts Within 2 Months
FOOD HACK for Weight Loss
A Simple Cooking Technique That Cuts The Calories & Glycemic
Impact In Rice, Pasta, And Potatoes In Half
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.
References
(1) Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG).
Singh NA1, Mandal AK2, Khan ZA3.(PubMed)
(2) Neuroprotective Activity of (-)-Epigallocatechin Gallate against Lipopolysaccharide-Mediated Cytotoxicity by Liu JB1, Zhou L1, Wang YZ2, Wang X2, Zhou Y2, Ho WZ3, Li JL2.(PubMed)
(3) Green tea compound epigallo-catechin-3-gallate (EGCG) increases neuronal survival in adult hippocampal neurogenesis in vivo and in vitro by Ortiz-López L1, Márquez-Valadez B2, Gómez-Sánchez A1, Silva-Lucero MD3, Torres-Pérez M1, Téllez-Ballesteros RI1, Ichwan M4, Meraz-Ríos MA5, Kempermann G6, Ramírez-Rodríguez GB7.(PubMed)
Singh NA1, Mandal AK2, Khan ZA3.(PubMed)
(2) Neuroprotective Activity of (-)-Epigallocatechin Gallate against Lipopolysaccharide-Mediated Cytotoxicity by Liu JB1, Zhou L1, Wang YZ2, Wang X2, Zhou Y2, Ho WZ3, Li JL2.(PubMed)
(3) Green tea compound epigallo-catechin-3-gallate (EGCG) increases neuronal survival in adult hippocampal neurogenesis in vivo and in vitro by Ortiz-López L1, Márquez-Valadez B2, Gómez-Sánchez A1, Silva-Lucero MD3, Torres-Pérez M1, Téllez-Ballesteros RI1, Ichwan M4, Meraz-Ríos MA5, Kempermann G6, Ramírez-Rodríguez GB7.(PubMed)
(4) Green Tea Consumption and the Risk of Incident Dementia in Elderly Japanese: The Ohsaki Cohort 2006 Study by Tomata Y1, Sugiyama K2, Kaiho Y2, Honkura K2, Watanabe T2, Zhang S2, Sugawara Y2, Tsuji I2(PubMed)
(5) Green tea (-)epigallocatechin-3-gallate reverses oxidative stress and reduces acetylcholinesterase activity in a streptozotocin-induced model of dementia by Biasibetti R1, Tramontina AC, Costa AP, Dutra MF, Quincozes-Santos A, Nardin P, Bernardi CL, Wartchow KM, Lunardi PS, Gonçalves CA.(PubMed)
(6) Coffee, tea, and caffeine consumption and prevention of late-life cognitive decline and dementia: a systematic review by Panza F1, Solfrizzi V, Barulli MR, Bonfiglio C, Guerra V, Osella A, Seripa D, Sabbà C, Pilotto A, Logroscino G.(PubMed)
(5) Green tea (-)epigallocatechin-3-gallate reverses oxidative stress and reduces acetylcholinesterase activity in a streptozotocin-induced model of dementia by Biasibetti R1, Tramontina AC, Costa AP, Dutra MF, Quincozes-Santos A, Nardin P, Bernardi CL, Wartchow KM, Lunardi PS, Gonçalves CA.(PubMed)
(6) Coffee, tea, and caffeine consumption and prevention of late-life cognitive decline and dementia: a systematic review by Panza F1, Solfrizzi V, Barulli MR, Bonfiglio C, Guerra V, Osella A, Seripa D, Sabbà C, Pilotto A, Logroscino G.(PubMed)
(7) The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer's disease: an overview of pre-clinical studies and translational perspectives in clinical practice by Cascella M#1, Bimonte S#1, Muzio MR2, Schiavone V3, Cuomo A1.(PubMed)
(8) Simultaneous manipulation of multiple brain targets by green tea catechins: a potential neuroprotective strategy for Alzheimer and Parkinson diseases by Mandel SA1, Amit T, Weinreb O, Reznichenko L, Youdim MB.(PubMed)
(9) Effects of caffeic acid on learning deficits in a model of Alzheimer's disease by Wang Y1, Wang Y2, Li J1, Hua L3, Han B1, Zhang Y1, Yang X3, Zeng Z3, Bai H3, Yin H1, Lou J3.(PubMed)
(10) Caffeic acid attenuates oxidative stress, learning and memory deficit in intra-cerebroventricular streptozotocin induced experimental dementia in rats by Deshmukh R1, Kaundal M2, Bansal V2, Samardeep2(PubMed).
(8) Simultaneous manipulation of multiple brain targets by green tea catechins: a potential neuroprotective strategy for Alzheimer and Parkinson diseases by Mandel SA1, Amit T, Weinreb O, Reznichenko L, Youdim MB.(PubMed)
(9) Effects of caffeic acid on learning deficits in a model of Alzheimer's disease by Wang Y1, Wang Y2, Li J1, Hua L3, Han B1, Zhang Y1, Yang X3, Zeng Z3, Bai H3, Yin H1, Lou J3.(PubMed)
(10) Caffeic acid attenuates oxidative stress, learning and memory deficit in intra-cerebroventricular streptozotocin induced experimental dementia in rats by Deshmukh R1, Kaundal M2, Bansal V2, Samardeep2(PubMed).
(11) Neuroprotective Properties of the Standardized Extract from Camellia sinensis (Green Tea) and Its Main Bioactive Components, Epicatechin and Epigallocatechin Gallate, in the 6-OHDA Model of Parkinson's Disease by Bitu Pinto N1, da Silva Alexandre B2, Neves KR3, Silva AH3, Leal LK3, Viana GS1.(PubMed)
(12) Green tea polyphenols prevent Parkinson's disease: in vitro and in vivo studies Dan Chen byIowa State University
(13) Green tea consumption affects cognitive dysfunction in the elderly: a pilot study by Ide K1, Yamada H2, Takuma N3, Park M4, Wakamiya N5, Nakase J6, Ukawa Y7, Sagesaka YM8.(PubMed)
(14) Consumption of green tea, but not black tea or coffee, is associated with reduced risk of cognitive decline by Noguchi-Shinohara M1, Yuki S1, Dohmoto C1, Ikeda Y1, Samuraki M1, Iwasa K1, Yokogawa M2, Asai K3, Komai K4, Nakamura H5,(PubMed)
(15) Effects of green tea consumption on cognitive dysfunction in an elderly population: a randomized placebo-controlled study by Ide K1, Yamada H2, Takuma N3, Kawasaki Y1, Harada S1, Nakase J4, Ukawa Y4, Sagesaka YM4.(PubMed)
(16) Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation by Kuo-Jen Wu,1 Ming-Tsuen Hsieh,1 Chi-Rei Wu,1 W. Gibson Wood,2 and Yuh-Fung Chen(Hindawi)
(17) Epigallocatechin-3-Gallate Attenuates Impairment of Learning and Memory in Chronic Unpredictable Mild Stress-Treated Rats by Restoring Hippocampal Autophagic Flux by Hong-Feng Gu1,2., Ya-Xiong Nie3., Qiao-Zhen Tong2., Ya-Ling Tang1 , Yang Zeng3 , Kai-Quan Jing3 , XiLong Zheng2,4, Duan-Fang Liao4(PLOS 1)
(18) Green tea extract: A potential cause of acute liver failure by Shreena S Patel, Stacey Beer, Debra L Kearney, Garrett Phillips, and Beth A Carter(PMC)
(19) Liver-related safety assessment of green tea extracts in humans: a systematic review of randomized controlled trials by T Isomura,1,2,3,4 S Suzuki,3,* H Origasa,4 A Hosono,3 M Suzuki,1 T Sawada,1 S Terao,1 Y Muto,1and T Koga(PMC)
(20) Neuroprotective effect of epigallocatechin-3-gallate against beta-amyloid-induced oxidative and nitrosative cell death via augmentation of antioxidant defense capacity by Kim CY1, Lee C, Park GH, Jang JH.(PubMed)
(21) l-Theanine, an amino acid in green tea, attenuates beta-amyloid-induced cognitive dysfunction and neurotoxicity: reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-kappaB pathways by Kim TI1, Lee YK, Park SG, Choi IS, Ban JO, Park HK, Nam SY, Yun YW, Han SB, Oh KW, Hong JT.(PubMed)
(22) Epigallocatechin Gallate Attenuates β-Amyloid Generation and Oxidative Stress Involvement of PPARγ in N2a/APP695 Cells by Zhang ZX1, Li YB2, Zhao RP3.(PubMed)
(23) Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice by Rezai-Zadeh K1, Arendash GW, Hou H, Fernandez F, Jensen M, Runfeldt M, Shytle RD, Tan J.(PubMed)
(24) Diet and amyotrophic lateral sclerosis by Morozova N1, Weisskopf MG, McCullough ML, Munger KL, Calle EE, Thun MJ, Ascherio A.(PubMed)
(25) Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis by Xu Z1, Chen S, Li X, Luo G, Li L, Le W.(PubMed)
(26) The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice by Koh SH1, Lee SM, Kim HY, Lee KY, Lee YJ, Kim HT, Kim J, Kim MH, Hwang MS, Song C, Yang KW, Lee KW, Kim SH, Kim OH.(PubMed)
(12) Green tea polyphenols prevent Parkinson's disease: in vitro and in vivo studies Dan Chen byIowa State University
(13) Green tea consumption affects cognitive dysfunction in the elderly: a pilot study by Ide K1, Yamada H2, Takuma N3, Park M4, Wakamiya N5, Nakase J6, Ukawa Y7, Sagesaka YM8.(PubMed)
(14) Consumption of green tea, but not black tea or coffee, is associated with reduced risk of cognitive decline by Noguchi-Shinohara M1, Yuki S1, Dohmoto C1, Ikeda Y1, Samuraki M1, Iwasa K1, Yokogawa M2, Asai K3, Komai K4, Nakamura H5,(PubMed)
(15) Effects of green tea consumption on cognitive dysfunction in an elderly population: a randomized placebo-controlled study by Ide K1, Yamada H2, Takuma N3, Kawasaki Y1, Harada S1, Nakase J4, Ukawa Y4, Sagesaka YM4.(PubMed)
(16) Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation by Kuo-Jen Wu,1 Ming-Tsuen Hsieh,1 Chi-Rei Wu,1 W. Gibson Wood,2 and Yuh-Fung Chen(Hindawi)
(17) Epigallocatechin-3-Gallate Attenuates Impairment of Learning and Memory in Chronic Unpredictable Mild Stress-Treated Rats by Restoring Hippocampal Autophagic Flux by Hong-Feng Gu1,2., Ya-Xiong Nie3., Qiao-Zhen Tong2., Ya-Ling Tang1 , Yang Zeng3 , Kai-Quan Jing3 , XiLong Zheng2,4, Duan-Fang Liao4(PLOS 1)
(18) Green tea extract: A potential cause of acute liver failure by Shreena S Patel, Stacey Beer, Debra L Kearney, Garrett Phillips, and Beth A Carter(PMC)
(19) Liver-related safety assessment of green tea extracts in humans: a systematic review of randomized controlled trials by T Isomura,1,2,3,4 S Suzuki,3,* H Origasa,4 A Hosono,3 M Suzuki,1 T Sawada,1 S Terao,1 Y Muto,1and T Koga(PMC)
(20) Neuroprotective effect of epigallocatechin-3-gallate against beta-amyloid-induced oxidative and nitrosative cell death via augmentation of antioxidant defense capacity by Kim CY1, Lee C, Park GH, Jang JH.(PubMed)
(21) l-Theanine, an amino acid in green tea, attenuates beta-amyloid-induced cognitive dysfunction and neurotoxicity: reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-kappaB pathways by Kim TI1, Lee YK, Park SG, Choi IS, Ban JO, Park HK, Nam SY, Yun YW, Han SB, Oh KW, Hong JT.(PubMed)
(22) Epigallocatechin Gallate Attenuates β-Amyloid Generation and Oxidative Stress Involvement of PPARγ in N2a/APP695 Cells by Zhang ZX1, Li YB2, Zhao RP3.(PubMed)
(23) Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice by Rezai-Zadeh K1, Arendash GW, Hou H, Fernandez F, Jensen M, Runfeldt M, Shytle RD, Tan J.(PubMed)
(24) Diet and amyotrophic lateral sclerosis by Morozova N1, Weisskopf MG, McCullough ML, Munger KL, Calle EE, Thun MJ, Ascherio A.(PubMed)
(25) Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis by Xu Z1, Chen S, Li X, Luo G, Li L, Le W.(PubMed)
(26) The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice by Koh SH1, Lee SM, Kim HY, Lee KY, Lee YJ, Kim HT, Kim J, Kim MH, Hwang MS, Song C, Yang KW, Lee KW, Kim SH, Kim OH.(PubMed)
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