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Wednesday, April 10, 2024
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Methylene Blue Parkinson’s Disease

Methylene Blue Photobiomodulation And Depression

Methylene Blue for Cancer and Neurodegeneration

In an early study in 1983, MB was recognized as a potential method for manic depression . In their study, oral MB administration significantly improved the symptoms of 14 of 19 manic depressive patients for whom standard therapies failed . In line with this, MB was also shown to be an effective addition in the long-term treatment of depression in a double-blind clinical trial . Moreover, MB can work effectively even on severe depression. The symptoms of patients included in a controlled trial with severe depressive illness were significantly improved after receiving 15mg/dayMB treatment . Previous studies have also confirmed the efficacy of MB for the treatment of bipolar disorder . Furthermore, depressive-like behavior in both human patients and animal models can been observed after TBI . However, MB has been shown to inhibit this depressive-like behavior .

These improvements may be explained mechanistically by the role of nitric oxide , an unconventional gaseous neurotransmitter, in mood disorders and by the selective inhibition of nitric oxide synthase . Not only does MB inhibit NOS in the brain, but it also affects other heme-containing enzymes including various cytochromes .

Methylene Blue Induced Macroautophagy In Vivo

To determine whether methylene blue induces macroautophagy in vivo, we treated mice with methylene blue for 2 weeks, and AMPK activation and LC3B type II conversion in the hippocampus and cortex were then examined. As shown in Figures 5 and 6, no significant change of AMPK protein level in the hippocampus and cortex was found upon methylene blue treatment. However, AMPK phosphorylation was dramatically enhanced by methylene blue, especially in high dose-treated group. AMPK1 and AMPK2 were also significantly increased after methylene blue treatment in a dose-dependent manner. ACC phosphorylation was promoted in high dose group. Similar to in vitro data, phosphorylation of mTOR was not significantly altered in either methylene blue-treated group. Compared with vehicle-treated group, LC3B type II level was dramatically elevated, suggesting enhanced autophagosome formation in methylene blue-treated groups. In the SVZ, however, none of these signal pathways was altered after methylene blue treatment, indicating that the methylene blue might not affect neural stem/progenitor cells . LC3B conversion also showed differences in distinct brain areas. Methylene blue increased LC3B type II in hippocampi and cortex while slightly decreased LC3B type II in SVZ of methylene blue-treated mice. Taken together, these data demonstrated that methylene blue can induce macroautophagy in hippocampus and cortex through AMPK but not mTOR pathway in vivo.

Mitochondrial Dysfunction In Parkinsons Disease

PD has been recognized as the second most common neurodegenerative disorder and is characterized by a progressive loss of dopaminergic neurons and the presence of Lewy bodies . Increasing evidence supports mitochondrial dysfunction as one of the main contributors to PD pathogenesis . A study on single neurons from idiopathic PD patients found that the abundances of Complex I and II were typically reduced . Inhibition of Complex I has been shown to induce dopaminergic neurodegeneration in humans, flies, and rodents, indicating a critical role for mitochondrial dysfunction in PD . In line with this, oxidative damage has been found in postmortem brain samples from PD patients .

Furthermore, certain mitochondria-related gene mutations capable of inducing mitochondrial dysfunction have been shown to cause familial forms of PD . Mutations in numerous genes, including SNCA, LRRK2, Parkin, PINK1, and ATP13A2, have been recognized as monogenic causes of familial PD . These mutations have been directly associated with mitochondrial dysfunction . Additionally, mtDNA in single neurons from idiopathic PD patients presented an increased number of multiple deletions on the background of a common deletion . Consistently, an accumulation of mtDNA mutations and reduced mtDNA copy numbers were found in the substantia nigra from sporadic PD patients . However, the increased mtDNA copy number seen with age in controls was not found in PD patients .

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Neuroprotective Effects Of Methylene Blue

Several reports show that methylene blue is able to minimize the symptoms of the cardia arrest and associated brain pathology . The mechanism underlying the neuroprotective effect of MB appears to be related to its electron cycling property and reduction-oxidation capacity. MB also enhances the mitochondrial electron transport chain pathways . Facilitating the release of O2 from the methemoglobin in the case of methemoglobinemia provide another explanation for the positive effect of MB in neuroprotection following injuries-induced hypoxia . MB also ameliorates the neuronal tissue metabolism, blood supply, potentiates synaptic functions and neuronal conduction through regulating glucose and oxygen utilization in ischemic neuronal tissues . In rats preconditioned with mild TBI, treatment with MB induced a significant reduction in the lesion size, improved the cognitive behaviors, and attenuated in the neuronal damages . Using MB alone or in combination with other therapies for the treatment of neurodegenerative disease such as Parkinson’s disease or Alzheimer’s disease resulted in significant improvements in behavior and attenuation in brain pathology .

Antonio C. Tedesco, … Priscila da Costa Carvalho de Jesus, in, 2017

Mucuna Pruriens For Parkinsons Disease And Lewy Body Dementia

Methylene Blue Capsules Nootropics Supercharge

Mucuna pruriens is a bean that is eaten in certain parts of Central America, India, the Philippines, Nigeria, Ghana, Brazil, and Malawi as part of the human diet. It has been in use as an important nitrogen-fixing agricultural product throughout the world including in the United States during the early part of the 1900s through about 1965. Mucuna beans contain high levels of L-Dopa, a precursor that the brain uses to manufacture dopamine.

In 1960, scientists discovered that dopamine deficiency was one of major contributing factors in the development of Parkinsons Disease symptoms. Levodopa or L-Dopa was first administered to patients in 1961 and doctors discovered that dramatic improvements occurred when patients were given increasing amounts of L-Dopa over long periods of time.

Unfortunately, beginning in 1975, carbidopa was added to the L-Dopa to reduce nausea. Thereafter Levodopa, which is still referred to as L-Dopa by doctors, was no longer a medication made of L-Dopa, the dopamine precursor molecule, but rather, a medication that consisted of L-Dopa and Carbidopa.

The tragedy is that L-Dopa was beneficial to Parkinsons disease patients, but in 1975, with the addition of Carbidopa, L-Dopa/Levodopa became famous for the fact that it created irreversible dyskinesias with long-term use.

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Oxygen Radical Absorbance Capacity Assay

The ORAC-FL method of Ou et al., partially modified by Dávalos et al. was followed, using a FLUOStar Optima microplate reader with 485-P excitation and 520-P emission filters. 2,2-Azobis- dihydrochloride , -6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid and fluorescein were purchased from Sigma-Aldrich. The reaction was carried out at 37 °C in 75mMK,Na phosphate buffer , and the final reaction mixture was 200µL. The tested compounds and Trolox standard were dissolved in DMSO to 10mM and further diluted in 75mMK,Na phosphate buffer . The final concentrations were 0.11µM for the test compounds and 16µM for Trolox. The blank was composed of 20µL 75mMK,Na phosphate buffer containing 2% DMSO, 120µL FL and 60µL AAPH, and was added in each assay. Antioxidant and FL solutions were placed in a black 96-well microplate and were pre-incubated for 15min at 37 °C. AAPH solution was then added rapidly using a multichannel pipette. The fluorescence was recorded every minute for 100min. A Trolox standard curve was also obtained in each assay. All reactions were carried out in triplicate and at least three different assays were performed for each sample.

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Health Benefits Of Methylene Blue

Used as both a dye and a medicinal treatment, methylene blue possesses a wide range of effective applications. The compound is considered a mild antiseptic, so it can be used to kill bacteria in the body, particularly in conjunction with other treatments. These and other properties make it an effective treatment for a variety of other conditions as well.

Methylene blue is often used as a treatment for urinary tract infections and other mild infections in conjunction with other treatments. Additionally, the compound can be used to treat malaria, cancer, skin conditions including psoriasis, Alzheimers disease, and cyanide as well as carbon monoxide poisoning. It is also used as a treatment for parasites, swine flu, and Parkinsons disease.

While several applications for the treatment have already been identified, it is likely that continued research will reveal more applications for methylene blue. In any case, care must be taken when using the treatment to prevent interactions and adverse effects associated with overconsumption.

Children’s Hospital Oakland Scientist Finds Potential Alzheimer’s Cure In Century

My Parkinson’s Story: Exercise

First study of its kind on a century-old drug could lead to new treatment for Alzheimer’s and Parkinson’s

Children’s Hospital & Research Center Oakland

A paper on the methylene blue study, conducted by Hani Atamna, PhD, and a his team at Children’s, was published in the March 2008 issue of the Federation of American Societies for Experimental Biology Journal. Dr. Atamna’s research found that methylene blue can prevent or slow the decline of mitochondrial function, specifically an important enzyme called complex IV. Because mitochondria are the principal suppliers of energy to all animal and human cells, their healthy function is critical.

“The results are very encouraging,” said Dr. Atamna. “We’d eventually like to try to prevent the physical and cognitive decline associated with aging, with a focus on people with Alzheimer’s disease. One of the key aspects of Alzheimer’s disease is mitochondrial dysfunction, specifically complex IV dysfunction, which methylene blue improves. Our findings indicate that methylene blue, by enhancing mitochondrial function, expands the mitochondrial reserve of the brain. Adequate mitochondrial reserve is essential for preventing age-related disorders such as Alzheimer’s disease.”

About Children’s Hospital & Research Center Oakland

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Interesting Methylene Blue Dosing Story

So… they did a trial with Methylene Blue for AD back in 2014 core.ac.uk/reader/29151100 and determined the minimum effective dose was 138 mg . They also found it was hard to stomach 138 mg, but if you took it with food then you absorbed less.

So… they did another trial in 2016 ncbi.nlm.nih.gov/pmc/articl… with LMTM for AD. This time they gave one group 150 mg a day, another group 250 mg a day, and they gave the control arm 8 mg a day JUST TO TURN THEIR PEE BLUE SO THEY WOULD NOT KNOW THEY WERE THE CONTROL ARM. They figured 8 mg a day would not skew anything as the 2014 study had already shown that 69 mg was much less effective than 138 mg.

Here is the interesting part: In the 2016 study, the control group taking 8 mg a day did just as well as the 150 mg and 250 mg a day groups! Except the 150 and 250 mg groups had a bunch of gastrointestinal issues

Rat Liver Mitochondria Isolation

All experiments with animals were in compliance with the Guidelines for Animal Experiments at the Institute of Physiologically Active Compounds of the Russian Academy of Science . Rat liver mitochondria were isolated from Wistar strain male rats aged 3.54 months old . The rats were fasted overnight, then anesthetized by carbon dioxide and decapitated using a guillotine. The liver was quickly removed and homogenized in an ice-cold isolation buffer . Then rat liver mitochondria were isolated by conventional differential centrifugation. The mitochondrial protein concentration was determined using a biuret procedure with bovine serum albumin as the standard.

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In Vitro Ache Bche And Cae Inhibition

Acetylcholinesterase , butyrylcholinesterase , carboxylesterase , acetylthiocholine iodide , butylthiocholine iodide , 5,5-dithiobis- , 4-nitrophenyl acetate , were purchased from Sigma-Aldrich .

AChE and BChE activities were measured by the Ellman method as described earlier. The assay solution consisted of 0.1MK/Na phosphate buffer pH 7.5, 25°C with the addition of 0.33mM DTNB, 0.02 unit/mL of AChE or BChE, and 1mM of substrate . The assays were carried out with a reagent blank containing all components except AChE or BChE to account for non-enzymatic hydrolysis of substrate. In addition, an enzyme blank was included that contained all components except substrate to account for non-substrate sulfhydryl groups. The activity of CaE was determined spectrophotometrically by the release of 4-nitrophenol at 405 nm. The assay solution consisted of 0.1MK/Na phosphate buffer pH 8.0, 25°C with the addition of 1mM 4-nitrophenyl acetate and 0.02 unit/mL of CaE. Assays were carried out with a blank containing all components except CaE.

Role Of Methylene Blue In Trauma Neuroprotection And Neuropsychiatric Diseases

Methylene Blue (Solution)  G2Gsources

Volume 15, Issue 8, 2016

Page: Pages: 11

Abstract

The prevalence of central nervous system trauma, neurodegenerative andpsychiatric diseases has significantly increased in recent years. Most of thesediseases show multifactorial causes and several progression mechanisms. The searchfor a medication which positively interferes in these mechanisms and therebychanges the course of these diseases is of great scientific interest. The aim of thepresent review is to assess current literature on the possible role of methylene blue in the central nervous system due to the increasing number of citations in spiteof the few articles available on the subject which suggest growing interest in theprotective effects of MB on the central nervous system. Searches were performed onPubMed and Thomson Reuters Web of Knowledge. Therefore, we provide anoverview of existing articles concerning: 1) MB actions 2) MB neuroprotection and cardiac arrest 3)MB neuroprotection and degenerative brain diseases 4) MB neuroprotection and psychiatric diseases.PubMed was chosen because it holds the highest number of articles on the subject, Thomson Reuterswas chosen due to its functionality which evaluates citations through analytic graphs. We conclude thatMB has a beneficial effect and acts through many mechanisms and pathways of the central nervoussystem, being a potential alternative for the treatment of many neurodegenerative and psychiatricdiseases.

CNS & Neurological Disorders – Drug Targets

Affiliation:

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How To Use Methylene Blue As A Covid Cure

DISCLAIMER: Always consult a doctor before undergoing treatment of any kind.

DO NOT USE METHYLENE BLUE IF YOU HAVE A G6PD DEFICIENCY, A LIVER, OR A KIDNEY DISORDER. DO NOT USE METHYLENE BLUE IF YOU ARE PREGNANT OR LACTATING.

IMPORTANT NOTE: Scientists have recently realized that COVID-19 need to be treated in 2 phases. Phase 1 occurs during the first 2-3 days of acute infection when symptoms are not as severe. During this initial phase of infection, you can use Methylene Blue as an at-home COVID treatment . During Phase 2 of the infection, when coughing begins, it is vital to supplement with Vitamin B3 at no less than 3000 mg per day . Take medicines to counteract the effects of a cytokine storm during phase II. We provide a list of potential options that you can use to treat a cytokine storm at home.

Consider using a Methylene Blue, Vitamin C, and NAC protocol for Phase 1 treatment and then continue with Methylene Blue through Phase 2 for COVID-19. Methylene Blue can be cycled with Chlorine Dioxide Solution to rebalance the body and recover during Long COVID or Post-COVID Vaccine Syndrome also.

Methylene Blue Photobiomodulation And Stroke

Another neurological disorder for which MB and PBM has been proposed is stroke . In a focal cerebral ischemia rat model, behavioral results were significantly improved after chronic oral MB treatment . Further studies demonstrated its beneficial role in decreasing total lesion volume, cerebral edema, and gray and white-matter damage, all of which contributed to the improvement of behavioral results . Lin et al., demonstrated that MB treatment was able to improve the activity of mitochondrial Complexes I, II, and III and significantly increase both oxygen consumption and glucose uptake in HT22 cells, a well-known neuronal cell line . Their in vivo experimental results indicated that cerebral global glucose uptake and blood flow were significantly increased in animals treated with MB . Furthermore, an in vitro study found that oxygen consumption rate increased after MB treatment even under the inhibitory effect of Complex I, III, and V inhibitors . In addition, neuronal ATP production has been shown to improve with MB treatment . In a MCAO rat model, the decreased activity of Complex I, III, and IV after ischemia/reperfusion injury contributed to decreased mitochondrial function, which was restored with a low-dose of MB .

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Mitochondrial Dysfunction In Alzheimer S Disease

Alzheimers Disease is a progressive, age-dependent neurodegenerative disorder, characterized by progressive impairment of learning and memory, formation of neurofibrillary tangles , and extracellular deposition of amyloid- . In addition to these pathological hallmarks , numerous studies have indicated that mitochondrial abnormalities are involved in the development of AD. For example, hypometabolism, decreased cerebral blood flow, decreased oxygen extraction, and decreased oxygen utilization have been observed in AD patients . In addition, increased oxidative stress and ROS production have also been observed in the brains of AD patients . The observed increase in ROS generation is capable of inducing DNA, proteins, and lipid damage, a typical pathological signature in AD neural tissue .

In addition to decreased regional blood flow and oxygen utilization, an impaired balance of mitochondrial fission and fusion has also been observed in the brains of AD patients . The expression of mitochondrial fusion proteins, such as Opa1, Mfn1, and Mfn2, were downregulated, while the levels of the fission proteins Drp1, Fis1, Mff, and Mief were upregulated in AD, suggesting that an elevated ratio of fission over fusion proteins may have been contributing to mitochondrial and neuronal dysfunction .

How Do I Find A Compounding Pharmacy In Us

Brain Boosting Methylene Blue || Benefits, Dosing, & Side Effects

Another way is by utilizing the Alliance for Pharmacy Compoundings website. Enter your city and state, and their directory will point you to nearby compounding pharmacies.

You can also find a compounding pharmacy by using the Professional Compounding Centers of Americas website. Enter your zip code or your city and state to find one.

And remember, your local community pharmacy may be able to compound your medication. If youre unsure, ask your pharmacist.

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