Obesity-induced cognitive decline: Role of brain oxidation and tocotrienols

Your doctor has had a long time to come up with a protocol for tocotrienols. Did they? Or were they incompetent in this also like they were in everything else about stroke recovery? Did they get human testing initiated?

• tocotrienols (10 posts to April 2011)

 

Obesity-induced cognitive decline: Role of brain oxidation and tocotrienols

Health Topics mentioned in this article Obesity

Alzheimers Disease

Cognitive Impairment Researchers from Shibaura Institute of Technology, Japan investigated the impact of HFSD on mice and found that tocotrienols (T3s), a form of vitamin E, show promise in protecting against cognitive decline associated with obesity, highlighting its therapeutic potential.

Obesity has become a pressing worldwide health issue, with rates steadily rising over recent decades. Beyond its well-documented associations with physical health issues, such as cardiovascular disease and diabetes, obesity has also been linked to cognitive decline, including conditions like Alzheimer's disease and Parkinson's disease. Understanding the complex mechanisms underlying this cognitive impairment is crucial for developing effective interventions. In a study published in the International Journal of Molecular Sciences, Assistant Professor Yugo Kato from Tottori University and Shibaura Institute of Technology, Professor Koji Fukui from Shibaura Institute of Technology and their team offer insights into potential solutions.The study investigated the neuroprotective effects of tocotrienols (T3s) in mitigating the adverse impact of diet-induced obesity on brain function."Our goal is to combat obesity-related diseases using natural compounds and thereby reduce the prevalence of conditions like dementia among individuals affected by obesity," says Prof. Kato.

T3s are a group of naturally occurring chemical compounds belonging to the vitamin E family. Past studies have revealed that T3s have neuroprotective and anti-obesity properties. Additionally, they have also been shown to pass through the blood-brain barrier and enter cells to produce antioxidant effects. However, little is known about how T3s contribute to the decline in brain function brought on by obesity.

Quality Settings 12 Years of Data Link Popular Diet to Brain BoostHigh Adolescent BMI Linked With Chronic Kidney Disease, Study Warns To address this gap, the team conducted a comprehensive investigation using a mouse model system. They employed a meticulous experimental design, with C57BL/6 male mice subjected to either a high-fat, high-sucrose diet (HFSD) or a control diet, supplemented with or without T3s. In the initial phase of the study, the team evaluated the anti-obesity effects of T3s. To do so, they incorporated a 50mg T3s mixture into 100g of both experimental diets, namely the control and HFSD. Key parameters, including body weight, fat deposition, serum cholesterol, triglyceride, and glucose concentrations, were assessed alongside cognitive function using the Morris water maze and Y-maze tests. Additionally, markers of oxidative stress and proteomic changes in the cortex were analyzed to gain deeper insights into the underlying mechanisms.The results of the study were highly promising. While HFSD feeding induced obesity in the mice, supplementation with T3s did not mitigate weight gain. However, T3s treatment demonstrated a significant improvement in cognitive function, as evidenced by enhanced learning ability in HFSD-fed mice. Furthermore, the study revealed the role of oxidative stress in obesity-induced cognitive decline, with HFSD-fed mice exhibiting increased brain oxidation levels. Remarkably, T3s treatment appeared to mitigate this oxidative stress, suggesting a potential mechanism for their neuroprotective effects. Additionally, contrary to expectations, the team found that respiratory metabolism decreased and the temperature around brown adipose tissue increased in mice fed with HFSD. This unexpected finding suggests that HFSD may have a complex impact on metabolic processes and temperature regulation in the body."Lastly, we wanted to examine the protein change associated with the consumption of the HFSD. So, we performed a quantitative proteomic analysis of the mouse cortex. Our focus was on the proteins that were expressed differently between the HFSD and control groups," explains Prof. Kato. They discovered that in comparison to the control group, obesity brought on by HFSD feeding changed 12 proteins, and mice treated with T3s showed considerable prevention of these changes. In conclusion, this study represents a significant step forward in our understanding of the intricate relationship between obesity and cognitive decline. By uncovering the potential benefits of T3s in preserving cognitive function, the research opens up new avenues for therapeutic interventions targeting neurodegenerative diseases associated with obesity.More information: Yugo Kato et al, Tocotrienols Prevent the Decline of Learning Ability in High-Fat, High-Sucrose Diet-Fed C57BL/6 Mice, International Journal of Molecular Sciences (2024). DOI: 10.3390/ijms25063561Provided by Shibaura Institute of TechnologyThis story was originally published on Medical Xpress. Subscribe to our newsletter for the latest sci-tech news

Tocotrienols Ameliorate Neurodegeneration and Motor Deficits in the 6-OHDA-Induced Rat Model of Parkinsonism: Behavioural and Immunohistochemistry Analysis

 You'll want your doctor to know how to apply this because of your risk of Parkinsons even though this is in rats.

Your risk of Parkinsons here:

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

Tocotrienols Ameliorate Neurodegeneration and Motor Deficits in the 6-OHDA-Induced Rat Model of Parkinsonism: Behavioural and Immunohistochemistry Analysis

Mangala Kumari 1,*, 

Premdass Ramdas 2, 

Ammu Kutty Radhakrishnan 3, 

Methil Kannan Kutty 4 

and Nagaraja Haleagrahara 5






Citation: Kumari, M.; Ramdas, P.;

Radhakrishnan, A.K.; Kutty, M.K.;

Haleagrahara, N.

1 Department of Anatomy, Division of Human Biology, School of Medicine, International Medical University,

Kuala Lumpur 57000, Malaysia

2 Division of Applied Biomedical Sciences and Biotechnology, School of Health Sciences, International Medical

University, Kuala Lumpur 57000, Malaysia; premdass_ramdas@imu.edu.my

3

Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway,Selangor 47500, Malaysia; Ammu.Radhakrishnan@monash.edu4 Department of Medicine, Lincoln University College, Kelana Jaya, Selangor 47301, Malaysia;methilkannan@gmail.com 5 College of Medicine and Dentistry, James Cook University, Townsville, QLD 4811, Australia; haleagrahara.nagaraja@jcu.edu.au * Correspondence: mangala_kumari@imu.edu.my 

Abstract: 

Parkinson’s disease (PD) is a debilitating neurodegenerative disease, which progresses

over time, causing pathological depigmentation of the substantia nigra (SN) in the midbrain due toloss of dopaminergic neurons. Emerging studies revealed the promising effects of some nutrient compounds in reducing the risk of PD. One such nutrient compound that possess neuroprotective effects and prevents neurodegeneration is tocotrienol (T3), a vitamin E family member. In the present study, a single dose intracisternal injection of 250 µg 6-hydroxydopamine (6-OHDA) was used to induce parkinsonism in male Sprague Dawley (SD) rats. Forty-eight hours post injection, the SD rats were orally supplemented with alpha (α)- and gamma (γ)-T3 for 28 days. The neuroprotective effects of α- and γ-T3 were evaluated using behavioural studies and immunohistochemistry (IHC).The findings from this study revealed that supplementation of α- and γ-T3 was able to ameliorate the motor deficits induced by 6-OHDA and improve the neuronal functions by reducing inflammation, reversing the neuronal degradation, and preventing further reduction of dopaminergic neurons in the SN and striatum (STR) fibre density. Keywords: vitamin E; tocotrienols; tyrosine hydroxylase; Parkinson’s disease; neurofunctions; 

1. Introduction 

Parkinson’s disease (PD) is the second most common progressive neurodegenerative disease in humans after Alzheimer’s disease ¹. The number of people with PD is estimated to be between 4 to 6 million in the most populous nations. Longitudinal meta-analysis data showed that the prevalence of PD steadily increased with age. Besides, the geographical prevalence is 2.5 times higher in people from Australia, Europe, and America compared to the individuals from Asia ². The selective loss of dopaminergic neurons in the pars compacta region of the substantia nigra (SN) of the midbrain and reduced striatal dopamine (DA) levels in the brain are the main pathological features that lead to the development of PD. These pathologies cause disturbances in the nigrostriatal dopaminergic pathway, which result in significant clinical abnormalities that manifest as motor and non-motor symptoms [3]. The motor symptoms of PD include tremor at rest, muscle rigidity, bradykinesia, postural instability, and autonomic disturbances. Some of the non-motor symptoms of PD include sleep disturbance, cognitive-related deficits, anosmia, depression, and gastrointestinal disorders [4].Neuroinflammation induced by activated neuroglia is also linked to the pathogenesisof PD. Activated neuroglia secretes pro-inflammatory cytokines, which further aggravate the disease [5]. Researchers postulated that drugs that target activated neuroglia and reducethe levels of pro-inflammatory cytokines in the brain are suitable candidate drug(s) for PD, as these types of drugs can reduce neuroinflammation and also alleviate neuronal oxidative stress [6]. Interestingly, some nutrients have been known to target activated neuroglia and have been reported to have profound effects in regulating the proinflammatory cytokines. Studies have revealed the role of some nutrients in reducing the risk of PD by preventingneurodegeneration or halting the disease progression ⁷.One such natural compound is tocotrienols (T3), a vitamin E family member, which is a naturally occurring fat-soluble vitamin ⁸. Tocotrienols are found naturally in annatto seeds, rice bran, and particularly palm oil and rice bran oil in which higher amounts of tocotrienols are present ⁹. Several studies have shown that T3 possesses many healthenhancing effects such as anti-cancer ^10,11, anti-proliferative ^12,13, anti-thrombotic ¹⁴, anti-inflammatory ¹⁵, antioxidant ¹⁶, and neuroprotective ^17,18 effects. Palm oilderived tocotrienol-rich fraction (TRF) has been reported to provide immense protection against cytotoxicity caused by oxidative stress (OS) in rat striatal cells ¹⁹. A recent systematic review on the safety and neuroprotective efficacy of palm-oil and TRF concluded that T3 could enhance the healthy animals’ cognitive function and attenuate OS ²⁰. According to Khanna et al., α-T3 exhibits cellular protection of the nerves through two main pathways: 12-lipoxygenase (LOX) and c-Src pathways ²¹. However, the reports on the neuroprotective effects of γ-T3 are minimal, in particular, the effects of γ-T3 supplementation on the 6-OHDA-induced rat model of parkinsonism are not available in the literature. A previous clinical trial showed the protective effects of mixed T3 in decreasing the progression of white matter lesions (WML) in 121 human volunteers ²². Moreover, palm vitamin E has achieved the “generally regarded as safe (GRAS)” status by the Food and Drug Administration (FDA), USA ²³. It is considered safe for consumption and has been attributed with many health-enhancing effects including brain health ²⁴. Animal models using various types of neurotoxins are popular tools that have been used for the study of PD over the past couple of decades and have imparted significant knowledge on the aetiology and pathogenesis of PD ²⁵. The specific target of neurotoxins in the animal models is the catecholaminergic neurons, which induce PD-related symptoms and pathology when impaired by neurotoxins. The neurotoxin 6-OHDA cannot cross the blood–brain barrier; hence, systemic administration will not cause parkinsonism ²⁶. The degree of the lesion with 6-OHDA depends on the route of administration (intracerebral or intracisternal), concentration, and the species used ^27–29. Hence, this study aimed to evaluate the neuroprotective efficacy of oral supplementation of isomers of T3 (α- and γ-T3) on the intracisternal 6-OHDA-injected rat model. With this study, we sought to determine whether isomers of T3 (α- and γ-T3) could reverse parkinsonian motor symptoms on 6-OHDA-injected SD rats and prevent the DA neuronal loss in agreement with the behavioural observation of the corresponding animals.

So Many Dietary Supplements – How Do You Choose?

The only ones I am taking right now are: Tocotrienols and Aged Garlic Extract. I have no clue what is in them because of the fucking stupidity of the US Congress in passing the Dietary Supplement Health and Education Act of 1994 (DSHEA): (DSHEA) defined dietary supplements as a category of food, which put them under different regulations than drugs. They are considered safe until proven otherwise. Caveat Emptor.

Aged garlic extract, 2400mg day

New study shows aged garlic extract can reduce dangerous plaque buildup in arteries

Palm tocotrienols can prevent brain cell death after stroke

I can probably stop this.

So Many Dietary Supplements – How Do You Choose?

 

Dietary tocotrienol/gamma-cyclodextrin complex increases mitochondrial membrane potential and ATP concentrations in the brain of aged mice

One of the reasons I take tocotrienol. Don't follow me, I know nothing about medicine.

Dietary tocotrienol/gamma-cyclodextrin complex increases mitochondrial membrane potential and ATP concentrations in the brain of aged mice  

Anke Schloesser1, Naoko Ikuta2, Keiji Terao2,3, Seiichi Matsugo4, Gerald Rimbach1* 
1Institute of Human Nutrition and Food Science, University of Kiel, Germany;  2Graduate School of Medicine, Kobe University, Japan;  3Cyclochem Bio Co., Ltd., Kobe, Japan;  4School of Natural System, Kanazawa University, Japan Email*: rimbach@foodsci.uni-kiel.de  
  Brain aging is accompanied by a decline in mitochondrial function. In vitro studies suggest that tocotrienols, including gamma- and delta-tocotrienol (T3), may exhibit neuroprotective properties [1]. However little is known about the effect of dietary T3 on mitochondrial function in vivo. In this study we monitored the effect of a dietary T3/gamma-cyclodextrin complex (T3CD) on mitochondrial membrane potential and ATP levels in the brain (cortex) of 21 month old aged mice. Mice were fed either control diet or a diet enriched with T3CD providing 100 mg T3 per kg diet for 6 months. Dietary T3CD significantly increased mitochondrial membrane potential and ATP levels as compared to controls. The increase of MMP and ATP due to dietary T3CD was accompanied by an increase in the protein levels of the mitochondrial transcription factor A (TFAM). Furthermore dietary T3CD slightly increased mRNA levels of superoxide dismutase, gamma-glutamyl cysteinyl synthetase and heme oxygenase 1 in the brain. Overall, present data suggest that T3CD increases TFAM, mitochondrial membrane potential and ATP synthesis in the brain of aged mice.

My supplement and diet regime

Do not follow this. There is no clinical proof that any of this works. There is initial research that I refer to but since we have NO leadership and NO strategy we will never find out what we should be eating post-stroke. Right now there is no way to easily measure if the endpoints of all this are working as expected.

1. chocolate - 80%+ cocoa, 2 pieces

CV prevention with dark chocolate 

2. beets, I do pickled because I can't stand cooked beets, they taste like my Moms. 4-5 oz.

New research suggests beets could help increase blood flow to the brain .

Beet Juice Beats Hypertension

 

Beet Juice Lowers Blood Pressure

3. tomatoes - fresh, not cooked

Lycopene in tomatoes reduces stroke risk by more than 50%

4. olive oil, used with balsamic vinegar for bread dipping.

Research proves that vegetables fried with olive oil have more healthy properties than boiled ones

Extravirgin olive oil consumption reduces risk of atrial fibrillation

To improve memory and thinking skills, try the Mediterranean diet with added olive oil and nuts

5 Healthy Eating Habits to Steal From Europeans

Olive oil cuts risk of stroke by 41 percent

5. Cranberry/pomegranate juice

Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation 

Cranberry juice consumption may protect against cardiovascular disease

Drinking low-calorie cranberry juice may help lower risk of heart disease, diabetes and stroke

6. greek yogurt - probiotics

Effect of Probiotics on Blood Pressure

Consumption of Fermented Milk Product With Probiotic Modulates Brain Activity

7. coffee - many cups

Moderate coffee drinking may be linked to reduced risk of death

Coffee associated with colon cancer survival

Good News: Coffee Could Be Cleaning Out Your Arteries.

Consuming one cup of coffee per day can decrease stroke risk by up to 20%.

 Does More Coffee Mean Less Arterial Plaque? -Arterial calcium lowest in healthy Korean adults with moderate-to-heavy coffee habits.

 

Coffee associated with colon cancer survival

How A Cup Of Coffee May Help People Manage Stress, Avoid Depression And Memory Loss

Coffee May Lower Your Risk of Dementia 

How coffee protects against Parkinson’s

Usual dose of caffeine has a positive effect on somatosensory related postural stability in hemiparetic stroke patients

Drinking Coffee Can Lower Alzheimer's Risk By 20%, All It Takes Is 3 Cups A Day

8. coconut oil, added to chai and for frying eggs, for grilled cheese sandwiches instead of margarine.

Evidence-Based Medicinal Properties of Coconut Oil - brain boosting  

9. Aged garlic extract, 2400mg day

New study shows aged garlic extract can reduce dangerous plaque buildup in arteries

10. Fish oil - Omega-3

Fish Oil Might Guard Against Loss of Brain Cells

Omega 3 fatty acid for the prevention of cognitive decline and dementia

11. tocotrienol

Palm tocotrienols can prevent brain cell death after stroke

12. almonds

New research shows almonds reduce the risk of heart disease

13. oatmeal

10 Foods to Calm Inflammation

14. watermelon, approximately 1 pound a day since I couldn't find juice.

Watermelon juice reverses hardening of the arteries  

15. Red wine

Can Wine Protect You From Having a Stroke?

16. Beer

The Close Ties Between Exercise and Beer

Women with moderate beer consumption run lower risk of heart attack

Guinness could really be good for you

If you're over 60, drink up: Alcohol associated with better memory

Beer compound could help fend off Alzheimer’s - hops

Dark beer is good for you, in moderation

I'm obviously not doing this very well since I'm still 35 lbs. above my ideal weight. I won't stop my dinners out and wine parties because the social connections are needed.

Molecular Basis of Vitamin E Action TOCOTRIENOL POTENTLY INHIBITS GLUTAMATE-INDUCED pp60c-Src KINASE ACTIVATION AND DEATH OF HT4 NEURONAL CELLS

From 2000 and I bet there was not a single followup human clinical trial.
Is this the solution to the glutamate poisoning problem in the neuronal cascade of death?
We'll never know because we have NO strategy or stroke leadership at all.
Molecular Basis of Vitamin E Action TOCOTRIENOL POTENTLY INHIBITS GLUTAMATE-INDUCED pp60c-Src KINASE ACTIVATION AND DEATH OF HT4 NEURONAL CELLS

1. Chandan K. Sen‡§,
2. Savita Khanna¶,
3. Sashwati Roy‡ and
4. Lester Packer¶

+ Author Affiliations

1. From the ^‡Lawrence Berkeley National Laboratory and ^¶Department of Molecular & Cell Biology, University of California, Berkeley, California 94720

Abstract

HT4 hippocampal neuronal cells were studied to compare the efficacy of tocopherols and tocotrienol to protect against glutamate-induced death. Tocotrienols were more effective than α-tocopherol in preventing glutamate-induced death. Uptake of tocotrienols from the culture medium was more efficient compared with that of α-tocopherol. Vitamin E molecules have potent antioxidant properties. Results show that at low concentrations, tocotrienols may have protected cells by an antioxidant-independent mechanism. Examination of signal transduction pathways revealed that protein tyrosine phosphorylation processes played a central role in the execution of death. Activation of pp60^c-Src kinase and phosphorylation of ERK were observed in response to glutamate treatment. Nanomolar amounts of α-tocotrienol, but not α-tocopherol, blocked glutamate-induced death by suppressing glutamate-induced early activation of c-Src kinase. Overexpression of kinase-active c-Src sensitized cells to glutamate-induced death. Tocotrienol treatment prevented death of Src-overexpressing cells treated with glutamate. α-Tocotrienol did not influence activity of recombinant c-Src kinase suggesting that its mechanism of action may include regulation of SH domains. This study provides first evidence describing the molecular basis of tocotrienol action. At a concentration 4–10-fold lower than levels detected in plasma of supplemented humans, tocotrienol regulated unique signal transduction processes that were not sensitive to comparable concentrations of tocopherol.

Abbreviations:

ROS

reactive oxygen species

DCF

dichlorofluorescein

DCFH-DA

dichlorodihydrofluorescein diacetate

PBS

phosphate-buffered saline

HPLC

high performance liquid chromatography

AAPH

2,2′-azobis[2-amidinopropane]hydrochloride

ERK

extracellular signal-regulated kinase

• Received August 19, 1999.
• Revision received January 12, 2000.

• The American Society for Biochemistry and Molecular Biology, Inc.

Vitamin E could prevent or reduce brain damage from stroke

Take this with a grain of salt for now. This is not standard vitamin E, you will need to specifically get the tocotrienol version. I talked about this 3 years ago here:

Not to be done without your doctors knowledge, you know how dangerous knowing something your doctor doesn't is.
Vitamin E could prevent or reduce brain damage from stroke

Earlier this year, Medical News Today reported on a study indicating that a daily dose of vitamin E may combat functional decline from Alzheimer’s disease. Now, a new study suggests the vitamin may help prevent or reduce brain damage during stroke.

Stroke occurs when an artery or blood vessel is blocked by clots or fatty build-ups, restricting blood flow to the brain. This deprives the brain of oxygen, which leads to brain cell death. Every year, around 15 million people worldwide have a stroke. Of these, 5 million are left permanently disabled.

After a stroke, a patient is usually treated with aspirin – an antiplatelet that works to stop the blood from clotting. In around 4% of stroke cases, patients are treated with tissue plasminogen activators – the only drug specific to stroke approved by the Food and Drug Administration – within 3 hours of the attack. This works by dissolving blood clots, therefore improving blood flow to the brain.

Study leader Dr. Cameron Rink, of The Ohio State University Wexner Medical Center, says it is “frustrating” that after 25 years of research and testing of more than 1,000 experimental neuroprotective drugs, there is no treatment available to patients to prevent stroke, rather than simply treat symptoms in the aftermath.

In animal studies, researchers found that tocotrienol supplements – a type of vitamin E – offers a “collateral” blood supply during stroke.

That is why, over the past 12 years, Dr. Rink has focused his research on finding such preventative treatment, and his latest study could be the most promising yet.

Tocotrienol improves blood supply

To reach their findings, Dr. Rink and colleagues conducted a series of animal studies that looked at the effects of tocotrienol supplements on blood vessels during stroke. Tocotrienol is a type of vitamin E found naturally in palm oil, which can block cholesterol production in the liver and reduce total blood cholesterol.

After 10 weeks’ worth of supplementation with the vitamin, the team found that it activated arteriogenesis – an increase in the diameter of existing arteries in response to oxygen demand. This process can prevent brain damage, as it effectively offers a “collateral” blood supply.

Commenting on the team’s findings, Dr. Rink says:

“We know that people who have good collaterals have better recovery from strokes. We think that tocotrienol helps improve the function of collaterals, which would offer someone better protection from an initial or secondary stroke.”

To investigate exactly how vitamin E activates arteriogenesis, Dr. Rink has created a laser capture microdissection method. This allows him to analyze minute pieces of brain tissue and blood vessels from exact areas where arteriogenesis occurs during stroke.

Using this technique, Dr. Rink can also analyze the activity of micro-RNAs during stroke. These are small pieces of non-coding DNA that switch off the production of proteins created by genes, therefore stopping the proteins from communicating with other cells. This may lead to an understanding of how tocotrienol influences genes during stroke.

At present, Dr. Rink is conducting a study of tocotrienol in stroke survivors to see if the vitamin may prevent or reduce brain damage from secondary strokes, which he notes can be more disabling than an initial stroke.

He concludes that one day, just like aspirin is recommended for cardiac patients, vitamin E may be used as a common treatment for stroke prevention.

May is National Stroke Awareness Month. In line with this campaign, Medical News Today have compiled a spotlight feature looking at the risks and warning signs of stroke and what is being done to increase awareness.

Research Article - The Antioxidant and Free Radical Scavenging Effects of Extracts of Seeds of Some Neglected Legumes of South-East Nigeria

This mainly is interesting for the line in it on tocotrienols, a Vitamin E variation.

Research Article - The Antioxidant and Free Radical Scavenging Effects of Extracts of Seeds of Some Neglected Legumes of South-East Nigeria

Tocotrienols have specialized roles in protecting neurons from damage,

cancer prevention and cholesterol reduction by

inhibiting the enzyme HMG-CoA reductase. Oral

consumption of tocotrienols is also proven to protect

against stroke associated brain damage [24]. 

24. Aruoma OI; Free radicals, oxidative stress and

12. Mpiana PT, Mudago V, Tshibangu DST, antioxidants in human health and disease.

Ngbolua KN, Shetorde OM, Mbala MB; In Journal of the American Oil Chemists Society, 

1998; 75(2): 199-212.  

Do not do anything without your doctors ok. Your doctor should have already read this in the Journal of the American Oil Chemists Society back in 1998. It's 16 years later, has any of this been translated into a stroke protocol?

More signs of total incompetence.

 

Research Shows Tocomin® May Improve Stroke Outcome - alpha-tocotrienol

Ok, but the mouse inflammation model does not match the human model. Everyone in stroke research should know that. And it's concerning that they are testing a commercial product. The previous studies showed that you had to have a certain level of this in your system prior to your stroke to help.

Research Shows Tocomin® May Improve Stroke Outcome - alpha-tocotrienol

New findings show alpha-tocotrienol may lead to improved stroke outcome by protecting neurons from cell death, according to a study published in the Journal of Cerebral Blood Flow and Metabolism.
Tocomin^® from Carotech, the alpha-tocotrienol used in the study, is a 12-Lox inhibitor that acts to confer neuroprotection post-stroke. A team of researchers at The Ohio State University Wexner Medical Center elucidated the mechanisms of microRNA precursor (miR29) in stroke-induced neuronal injuries. They showed that alpha-tocotrienol prevented miR29 loss at the infarct site during stroke.
 “Micro RNAs (miR) are small non-coding RNA molecules that play important role in regulating gene expression at the translation level, and miR29 is the micro RNA in the study of stroke etiology and in many other neurodegenerative disorders including Alzheimer’s Disease," said Savita Khanna, co-researcher of the study.
The miR29 family of genes, miR29a, miR29b1, miR29b2 (collectively miR29b) and miR29c, plays an important role in regulating gene expression. MiR29b is recognized as a neuronal survival factor. Specific loss of miR-29b at the infarct site after stroke leads to neuronal cell death. Prevention of such stroke-induced loss of miR-29b significantly improves stroke outcomes.
Researchers used the mouse stroke model, where mice were subjected to temporary middle-cerebral artery occlusion (MCAO), to induce stroke. At 48 hours after MCAO, there was a significant loss of miR29b at the infarct site.
Re-introducing miR29b at the infarct site decreased stroke-induced brain lesion by half compared to the control. In addition, the miR29b significantly improved post-stroke sensorimotor functions, where the cohort receiving miR29b had better agility and movement 48 hours post-stroke compared to control.
Then, researchers tested the efficacy of alpha-tocotrienol in the same mouse stroke model. Test mice were given 50 mg/kg body weight of alpha-tocotrienol and control mice were given vitamin E-stripped corn oil for 10 weeks before subjecting them to MCAO. The results showed that stroke-induced loss of miR29b was completely spared in the tocotrienol supplemented group, which resulted in smaller lesion size.
“I am excited with this new fifth checkpoint of tocotrienol in preventing stroke-induced injuries," said WH Leong, vice president of Carotech."It further strengthens the science of Tocomin^® for neuroprotection. In a stroke event, neuroprotective miR29b is loss due to the downstream product of 12-Lipoxygenase (12-Lox) called 12HETE, which leads to neuronal cell death. Tocomin^® is able to rescue miR29b by inhibiting 12-Lox."

Palm tocotrienols can prevent brain cell death after stroke

The title doesn't correspond to the article, it seems to reduce White matter lesions as a preventative rather than as a post stroke therapy.  Tocotrienols are a specialized form of vitamin E, you won't get them in standard drug store vitamins. No self-medication, that what your doctors are paid for.
I wrote about this a year and a half ago like this;
So here goes:

What are they? A natural component of Vitamin E that is found in barley, rice bran and palm oil products. Your standard vitamin E supplements only contain the tocopherols.
This report suggests that a level of this vitamin E can protect the brain after a stroke. But it takes about eight to 10 weeks of supplementation to build up to an adequate level in your system. For most Asians having a rice diet they would naturally have this.
Palm tocotrienols can prevent brain cell death after stroke

Researchers led by Professor Yuen Kah Hay of Universiti Sains Malaysia (USM) recently found that palm tocotrienols can protect brain cells in the event of a stroke.
“This breakthrough research suggests that taking 200mg of palm Researchers led by Professor Yuen Kah Hay of Universiti Sains Malaysia (USM) recently found that palm tocotrienols can protect brain cells in the event of a stroke.
“This breakthrough research suggests that taking 200mg of palm tocotrienols twice daily as a preventative can prevent brain cells from dying in the event of a stroke, which may translate to disability or survival benefits to the patients,” Professor Yuen said during a talk at a hotel here recently.
And considering stroke is the third biggest killer in Malaysia after heart disease and cancer, palm tocotrienols may bring benefits to the millions affected by this condition.
Professor Yuen and his team commenced the clinical trial after promising results were obtained in an American study which elucidated palm tocotrienols to be involved in the cell death signaling pathway to prevent neuronal cell death.
The researchers in America published their result after experimenting on genetically modified mice that are prone to stroke, as well as on canines, showing palm tocotrienols could minimize neuronal cell damage.
He said that 200 human volunteers with white matter lesions (WML), which are oxygen-starved brain cells, were recruited in the study led by him.
The placebo-controlled, randomized, double-blind clinical trial, which commenced in January, 2008, continued for two years.
At the end of the first year, the researchers found those taking 200mg of palm tocotrienols orally twice a day showed small increase in the WML volume, whereas those in the placebo group showed seven times more increase in WML volume.
“The placebo group continued to show further increases in the volume of lesions in the second year. Those on palm tocotrienols, however, showed a decrease.”
“The evidence we have now suggests that if people take it as a neuroprotective supplement, it can prevent brain cells from dying in the event of a stroke, and also stimulate the reconstruction of blood vessels after,” he said.
The encouraging results of the neuroprotective agent – palm tocotrienols, have led the Performance Management and Delivery Unit (PEMANDU) to fund a similar trial on diabetic patients, he said.
Meanwhile, USM researcher, Dr Enrico Magosso spoke on fatty liver and how this was a lifestyle disease.
“It is a progressive disease and affects between 10 percent and 30 percent of the world population. It is expected to become a major reason for transplant in the US, and patients with fatty liver are more likely to die from stroke,” he said.
He mentioned that in his study, he has found that tocotrienols has been effective in the prevention treatment of fatty liver.

Vitamin E May Pose Slight Bleeding-Stroke Risk

So who is going to collate all this info on supplements for survivors? We need the medical staff to step up to the plate. What about tocotrienols? being used for rehab 

Vitamin E May Pose Slight Bleeding-Stroke Risk.

People who take vitamin E supplements may be putting themselves at a slight increased risk for a hemorrhagic stroke, researchers report.

Some studies have suggested that taking vitamin E can protect against heart disease, while others have found that, in high doses, it might increase the risk of death. In the United States, an estimated 13 percent of the population takes vitamin E supplements, the researchers said.

“Vitamin E supplementation is not as safe as we may like to believe,” said lead researcher Dr. Markus Schurks, who’s with the division of preventive medicine at Brigham and Women’s Hospital in Boston.

“Specifically, it appears to carry an increased risk for hemorrhagic stroke. While the risk is low translating into one additional hemorrhage per 1,250 persons taking vitamin E, widespread and uncontrolled use of vitamin E should be cautioned against,” he added.

The report is published in the Nov. 5 online edition of the BMJ.

For the study, Schurks and his colleagues did a meta-analysis, which is a review of published studies, that looked at vitamin E and the risk for stroke.

There are basically two types of stroke: one where blood flow to the brain is blocked, called an ischemic stroke, and one where vessels rupture and bleed into the brain, called a hemorrhagic stroke. Of the two, hemorrhagic strokes are more rare, but more serious, the researchers noted.

The research team looked at nine trials that included 118,756 patients. Although none of the trials found an overall risk for stroke associated with vitamin E, there was a difference in the risk of the type of stroke.

The researchers found there were 223 hemorrhagic strokes among the 50,334 people taking vitamin E, compared with 183 hemorrhagic strokes among the 50,414 people taking a placebo. That’s a 22 percent increase in hemorrhagic stroke risk among vitamin E users, Schurks’s group noted.

However, for the risk of ischemic stroke, vitamin E was actually mildly protective, reducing the risk of ischemic stroke 10 percent, the researchers found.

Schurks said the absolute risk of having a hemorrhagic stroke linked to vitamin E is small — one additional hemorrhagic stroke for every 1,250 people taking the supplement.

Vitamin E may prevent one ischemic stroke in 476 people taking the supplement, the researchers added.

The researchers stressed that other ways of reducing the risk of strokes — such as lowering blood pressure, taking cholesterol-lowering drugs and living a healthy lifestyle — have much more impact on preventing ischemic stroke than vitamin E.

Dr. Larry B. Goldstein, director of the Duke University Stroke Center, said that “in addition to the studies included in this analysis, a large randomized trial of a combination of antioxidant vitamins, including vitamin E, in patients with vascular disease or diabetes found no effect on vascular events, including stroke, despite a significant increase in blood levels of the vitamins.”

There’s also some data suggesting that antioxidant vitamins might interfere with the effects of statin medications used to lower cholesterol levels in patients with vascular disease, he said.

“As there is no evidence of benefit and at least the possibility of harm, these vitamin supplements should generally be avoided, or at least their use should be discussed with a physician if being taken for a specific medical condition,” Goldstein said.

alpha tocotrienols and stroke

I hadn't really seen anything about this until I was contacted by a PR firm wondering if I wanted to blog on this. I tried asking, Why me? but she didn't respond.
So here goes:
What are they? A natural component of Vitamin E that is found in barley, rice bran and palm oil products. Your standard vitamin E supplements only contain the tocopherols.
This report suggests that a level of this vitamin E can protect the brain after a stroke. But it takes about eight to 10 weeks of supplementation to build up to an adequate level in your system. For most Asians having a rice diet they would naturally have this.
How one form of natural vitamin E protects brain after stroke

marketing websites here:
www.carotech.netwww.tocotrienol.orghttp://www.tocotrienol.org/images/stories/pdf_upload/Magazines/tocomin%20natural%20neuroprotective%20vitamin.pdf
I'm afraid that this is attempting to be the next statin blockbuster, so beware. Although for survivors it might be one more prevention. I'll wait until more trials are done.
It does talk about stopping glutamate damage which I discussed here;

Protecting the Brain from a Glutamate Storm

I'm more interested in acute phase intervention with this. Dr. Sen has proven that tocotrienols, taken orally, cross the blood-brain barrier.
None of this is going to help me, I need either hard neuroplasticity, neurogenesis or stem cells.