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Mitochondrial and Brain Stuff....New Discoveries and ?????

Discussion in 'The Epi-Paleo Diet' started by chocolate, Mar 27, 2012.

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    chocolate Silver

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    chocolate Silver


    Does this mean breathing controls it or it controls breathing? We are trying for a new conciousness right?

    Now I am seeing talk versus task signals. The liver talks and I don't know what else does. The breathing thing would be nice.... the metabolics just aren't one thing at a time.

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    PHILADELPHIA — Insulin resistance in the brain precedes and contributes to cognitive decline above and beyond other known causes of Alzheimer's disease, according to a new study by researchers from the Perelman School of Medicine at the University of Pennsylvania. Insulin is an important hormone in many bodily functions, including the health of brain cells. The team identified extensive abnormalities in the activity of two major signaling pathways for insulin and insulin-like growth factor in non-diabetic people with Alzheimer's disease. These pathways could be targeted with new or existing medicines to potentially help resensitize the brain to insulin and possibly slow down or even improve cognitive decline.
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    Bacteria could be significant cause of OCD

    Streptococcus bacteria, which cause "strep throat", scarlet fever and other infections, evade the immune system by making surface proteins that mimic human ones. The immune system eventually catches on and makes antibodies to the proteins – but these can then attack human tissue including the heart, joints and brain. This has long been known to cause heart disease and a nervous disorder called Sydenham's chorea.
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    chocolate Silver

    http://www.powersupplements.com/blog/784/alzheimer%E2%80%99s-sirtuin-protein/ its a supplement market but its a good article about siruitin activation and Alzheimer's, Huntington's, and Parkinsons.

    Researchers at the Massachusetts Institute of Technology (MIT) have conducted a study in mice that shows a promising new way to treat Alzheimer’s, Parkinson’s and Huntington’s Disease. The study focused on the role that Sirtuin, a protein in the body. played in neurodegenerative diseases. What they found was activating sirtuin suppressed the disease and that destroying sirtuin made the disease much worse.



    What in the World is Mitochondria?

    Every cell in our body has these amazing little cellular structures called mitochondria. The mitochondria are responsible for converting the nutrients from the food we eat into energy. Yes, the mitochondria have the daunting task of providing energy for every cell in our body, so we can eat, move, think, talk, breathe, etc.

    As we age the mitochondria can be destroyed and damaged and this leads to a host of problems. Dr. Sinclair, believing that Resveratrol may help repair damaged mitochondria, did an analysis of the liver of the mice to check for mitochondria content. Sure enough, the liver of the HCR (high calories resveratrol) mice had considerably more mitochondria than the livers of the HC mice.
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    Nature | News

    Sirtuin protein linked to longevity in mammals

    Male mice overproducing the protein sirtuin 6 have an extended lifespan.

    Heidi Ledford

    22 February 2012

    At last, a member of the celebrated sirtuin family of proteins has been shown to extend lifespan in mammals — although it’s not the one that has received the most attention and financial investment.

    Sirtuin genes and the proteins they encode have intrigued many researchers who study ageing ever since they were first linked to longevity in yeast. Results published today in Nature suggest that the overexpression of one gene, called sirtuin 6 (SIRT6), can lengthen lifespan in male mice by as much as 15.8%1.

    Male mice with boosted levels of the sirtuin protein SIRT6 could live longer.

    Getty Images

    For years, another member of the family, SIRT1, has hogged much of the spotlight because it is the mammalian member of the sirtuin clan most closely related to the longevity-linked yeast gene. Some researchers speculated that SIRT1 may also boost lifespan in mammals, and that it was the target of resveratrol, a compound found in red wine that had been linked to a variety of health benefits.

    David Lombard, a sirtuin researcher at the University of Michigan agrees with Miller, saying that it is important for researchers to directly address whether SIRT6 affects several of the conditions associated with ageing, such as cataract formation and declines in memory and mobility. Since the initial work with SIRT6-deficient mice was published, he notes, researchers have found that much of what initially seemed to be an accelerated rate of age-related degeneration may in fact be attributable to metabolic defects that cause extremely low blood-sugar levels.

    And why does SIRT6 affect males and females differently? Cohen’s lab is trying to piece that together, but for now he can only offer speculation. He notes that in the strain of mice his team used, females live about 15% longer than males and that overexpression of SIRT6 simply allowed the males to catch up to the females. Perhaps, then, SIRT6 is mimicking effects already seen in the females of this strain of mice. In this context, Rafael de Cabo, who studies ageing at the National Institute on Ageing in Baltimore, Maryland, notes that the expression of some proteins in the transgenic mice producing excess SIRT6 matched the expression of those proteins in normal, control female mice.

    The gist of the study, the way I understand it, is that the male rats age increased by abut 15 per cent, but it just made them equivalent in survival to the females. It's as though the females were maxed out already. Based on the toggling from male to female, I guess.
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    Researchers have identified a gene with a key role in neuronal survival

    Gene illustrationResearchers at the Institute of Neurosciences at Universitat Autònoma de Barcelona (INc-UAB) identified the fundamental role played by the Nurr1 gene in neuron survival associated with synaptic activity.

    The discovery, published in the Journal of Biological Chemistry, allows scientists to study a new target that could help to understand the relationship between alterations in neural connections, which are known to cause early cognitive deficit, and the neurodegeneration characteristic of Alzheimer’s disease.

    During the development of the brain, hundreds of thousands of neurons die if they do not establish the necessary connections – synapses – with their cell targets. The process of regulating neuron survival and death is fundamental in the organization of brain connections forming the adult brain.

    The effect of synaptic activity on the survival of these neurons however is not limited to the developing brain; it is also fundamental in the adult brain. The loss of synaptic activity, which results into the characteristic cognitive impairment seen in neurodegenerative diseases such as Alzheimer’s, precedes and contributes to the neuronal death observed in these pathologies. Despite the importance of this process, there is no exact knowledge of the molecular mechanisms implied in neuron survival generated by this activity.

    In the study directed by José Rodríguez Ã￾lvarez, researcher of the UAB Institute of Neurosciences, scientists determined the relation of a gene and the neuron survival regulated by synaptic activity. Through a massive analysis of gene activity, researchers identified several dozens of genes whose functions are regulated by this activity. Of all the genes, the research demonstrates the key role played by the Nurr1 gene in the survival of neurons.

    Among the discoveries made, researchers observed that when the activity of this gene is silenced, the neuron dies. The research concludes that this identification provides a better understanding into the relationship between early synaptic deficits and the posterior neurodegeneration observed in Alzheimer’s disease.
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    A ketogenic diet increases brain insulin-like growth factor receptor and glucose transporter gene expression.

    Cheng CM, Kelley B, Wang J, Strauss D, Eagles DA, Bondy CA.


    Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.


    A ketogenic diet suppresses seizure activity in children and in juvenile rats. To investigate whether alteration in brain IGF activity could be involved in the beneficial effects of the ketogenic diet, we examined the effects of this diet on IGF system gene expression in the rat brain. Juvenile rats were fed one of three different diets for 7 d: ad libitum standard rat chow (AL-Std), calorie-restricted standard chow (CR-Std), or a calorie-restricted ketogenic diet (CR-Ket). The calorie-restricted diets contained 90% of the rats' calculated energy requirements. The AL-Std diet group increased in weight, whereas the two CR groups merely maintained their weight during the 7-d diet. Glucose levels were significantly reduced in both CR groups compared with the AL-Std group, but only the CR-Ket group developed ketonemia. IGF1 mRNA levels were reduced by 30-50% in most brain regions in both CR groups. IGF1 receptor (IGF1R) mRNA levels were decreased in the CR-Std group but were increased in the CR-Ket diet group. Brain IGF binding protein (IGFBP)-2 and -5 mRNA levels were not altered by diet, but IGFBP-3 mRNA levels were markedly increased by the ketogenic diet while not altered by calorie restriction alone. Brain glucose transporter expression was also investigated in this study. Glucose transporter (GLUT) 4 mRNA levels were quite low and not appreciably altered by the different diets. Parenchymal GLUT1 mRNA levels were increased by the CR-Ket diet, but endothelial GLUT1 mRNA levels were not affected. Neuronal GLUT3 expression was decreased with the CR-Std diet and increased with the CR-Ket diet, in parallel with the IGF1R pattern. These observations reveal divergent effects of dietary caloric content and macronutrient composition on brain IGF system and GLUT expression. In addition, the data may be consistent with a role for enhanced IGF1R and GLUT expression in ketogenic diet-induced seizure suppression.
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    18 Apr 2012 - Scientists have created a simple new model of the human brain which reproduces the statistics of its complex network organization.

    Researchers at the University of Cambridge have developed a simple mathematical model of the brain which provides a remarkably complete statistical account of the complex web of connections between various brain regions. Their findings have been published this week in the journal Proceedings of the National Academy of Sciences (PNAS).

    The brain shares a similar pattern of connections with other complex networks such as social networks and the world wide web. However, until now, it was not known what rules were involved in the formation of the human brain network.

    The scientists, from the Behavioral and Clinical Neuroscience Institute in the Department of Psychiatry, and the National Institute of Mental Health in the US, discovered that the network can be modeled as a result of just two different competing factors: a distance penalty based on the cost of maintaining long-range connections between various brain regions and a second term modeling the preference for links between regions sharing similar input.

    Professor Ed Bullmore, lead author on the paper, explains the dynamic between the parameters they identified: “There is a huge amount of evidence that the wiring of brain networks tends to minimize connection costs. Less costly, short-distance connections are much more numerous than more costly, long-distance connections. So our model realistically includes a distance penalty on long-distance connections, which will tend to keep connection costs low.

    “However, we found that cost control alone was not enough to reproduce a wide range of network properties. To do that, we had to model an economical trade-off between cost control and another term which favoured new, direct connections between regions that shared similar input or were otherwise already indirectly linked.”

    The model not only increases our understanding of healthy brains, but the researchers believe it could also provide unique insight into disorders such as schizophrenia.

    Dr Petra Vertes, one of the authors of the paper, said: “Our model hints at possible mechanisms behind schizophrenia, which will be interesting to investigate further. We have been able to model the disease by tuning the parameters to allow a greater probability of connection between distant brain regions. This result echoes some prior neuroimaging results which suggest that brain networks in schizophrenia may be associated with an abnormal trade-off between connection costs and other topological properties of brain networks.”

    To watch a video which shows the pattern of connections that make up a network in the brain, please visit: http://www.youtube.com/watch?v=f3P15X_62xQ[/video]][video=youtube_share;f3P15X_62xQ]http://www.youtube.com/watch?v=f3P15X_62xQ[/video]
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    share digg


    Brain imagingA cellular protein called HDAC6, newly characterized as a gatekeeper of steroid biology in the brain, may provide a novel target for treating and preventing stress-linked disorders, such as depression and post-traumatic stress disorder (PTSD), according to research from the Perelman School of Medicine at the University of Pennsylvania.

    Glucocorticoids are natural steroids secreted by the body during stress. A small amount of these hormones helps with normal brain function, but their excess is a precipitating factor for stress-related disorders.

    Glucocorticoids exert their effects on mood by acting on receptors in the nucleus of emotion–regulating neurons, such as those producing the neurotransmitter serotonin. For years, researchers have searched for ways to prevent deleterious effects of stress by blocking glucocorticoids in neurons. However, this has proved difficult to do without simultaneously interfering with other functions of these hormones, such as the regulation of immune function and energy metabolism. more on the link
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    Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mice fed a ketone ester diet

    Published online before print February 23, 2012, doi: 10.1096/fj.11-200410

    We measured the effects of a diet in which d-β-hydroxybutyrate-(R)-1,3 butanediol monoester [ketone ester (KE)] replaced equicaloric amounts of carbohydrate on 8-wk-old male C57BL/6J mice. Diets contained equal amounts of fat, protein, and micronutrients. The KE group was fed ad libitum, whereas the control (Ctrl) mice were pair-fed to the KE group. Blood d-β-hydroxybutyrate levels in the KE group were 3-5 times those reported with high-fat ketogenic diets. Voluntary food intake was reduced dose dependently with the KE diet. Feeding the KE diet for up to 1 mo increased the number of mitochondria and doubled the electron transport chain proteins, uncoupling protein 1, and mitochondrial biogenesis-regulating proteins in the interscapular brown adipose tissue (IBAT). [18F]-Fluorodeoxyglucose uptake in IBAT of the KE group was twice that in IBAT of the Ctrl group. Plasma leptin levels of the KE group were more than 2-fold those of the Ctrl group and were associated with increased sympathetic nervous system activity to IBAT. The KE group exhibited 14% greater resting energy expenditure, but the total energy expenditure measured over a 24-h period or body weights was not different. The quantitative insulin-sensitivity check index was 73% higher in the KE group. These results identify KE as a potential antiobesity supplement.—Srivastava, S., Kashiwaya, Y., King, M. T. Baxa, U., Tam, J., Niu, G., Chen, X., Clarke, K., Veech, R. L. Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mice fed a ketone ester diet.

    brown fat

    electron transport chain

    sympathetic activity
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    Vitamin E decreases bone density


    Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption1, 2, 3. Osteoclasts are multinucleated cells that are formed by mononuclear preosteoclast fusion1, 2, 4, 5. Fat-soluble vitamins such as vitamin D are pivotal in maintaining skeletal integrity. However, the role of vitamin E in bone remodeling is unknown. Here, we show that mice deficient in α-tocopherol transfer protein (Ttpa−/− mice), a mouse model of genetic vitamin E deficiency6, have high bone mass as a result of a decrease in bone resorption. Cell-based assays indicated that α-tocopherol stimulated osteoclast fusion, independent of its antioxidant capacity, by inducing the expression of dendritic-cell–specific transmembrane protein, an essential molecule for osteoclast fusion, through activation of mitogen-activated protein kinase 14 (p38) and microphthalmia-associated transcription factor, as well as its direct recruitment to the Tm7sf4 (a gene encoding DC-STAMP) promoter7, 8, 9. Indeed, the bone abnormality seen in Ttpa−/− mice was rescued by a Tm7sf4 transgene. Moreover, wild-type mice or rats fed an α-tocopherol–supplemented diet, which contains a comparable amount of α-tocopherol to supplements consumed by many people, lost bone mass. These results show that serum vitamin E is a determinant of bone mass through its regulation of osteoclast fusion.
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    Studies have revealed that frataxin is an important mitochondrial protein for proper function of several organs. Yet in people with the disease, the amount of frataxin in affected cells is severely reduced. It is believed that the loss of frataxin makes the nervous system, heart, and pancreas particularly susceptible to damage from free radicals (produced when the excess iron reacts with oxygen). Once certain cells in these tissues are destroyed by free radicals they cannot be replaced. Nerve and muscle cells also have metabolic needs that may make them particularly vulnerable to this damage. Free radicals have been implicated in other degenerative diseases such as Parkinson's and Alzheimer's diseases.

    Based upon this information, scientists and physicians have tried to reduce the levels of free radicals, also called oxidants, using treatment with “antioxidants.” Initial clinical studies in Europe suggested that antioxidants like coenzyme Q10, vitamin E, and idebenone may offer individuals some limited benefit. However, recent clinical trials in the United States and Europe have not revealed effectiveness of idebenone in people with Friedreich’s ataxia, but more powerful modified forms of this agent and other antioxidants are in trials at this time. There is also a clinical trial to examine the efficacy of selectively removing excess iron from the mitochondria.
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