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Nathan Goodyear

Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

  • concussive brain injury is a major cause of neuropsychological disability in spite of no obvious neuronal death
  • TBI elicits oxidative damage to plasma membrane phospholipids
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain, where the DHA-containing phospholipids contribute to plasma membrane biogenesis and receptor signaling
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  • curcumin has potent anti-inflammatory and antioxidant activities that can function to reduce oxidative damage and cognitive deficits associated with neurological disorders
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction
  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus
  • previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
  • Our findings indicate that curcumin counteracted the TBI-related reduction in n-3 DPA.
  • curcumin may promote the conversion of n-3 DPA to DHA
  • the combination of both nutrients has been reported to produce anti-inflammatory action
  • the enhanced actions of curcumin and DHA in reducing cholesterol levels could be interpreted as preservation of levels of phospholipids in the plasma membrane
  • curcumin and DHA may contribute to reduce inflammation associated with the action of cholesterol in the pathology of TBI.
    Curcumin and DHA shown to protect against TBI through a reduction in inflammation and maintenance of brain phospholipid membranes.  BDNF is increases also.
Nathan Goodyear

Omega-3 Fats Critical to Brain Health After Traumatic Injury and Surgery - 0 views

    Just the press release, but DHA and EPA found to improve nerve cell survival, reduce neuroinflammation and decrease oxidative stress via "resolvins"
Nathan Goodyear

Dietary Supplementation With the Omega-3 Fatty Acid Docosahe... : Neurosurgery - 0 views

    Animal study finds pre-emptive DHA at 40 mg/kg reduced injury response during medically induced TBI.  Not only can DHA be used with TBI, but this study suggests it can be used in a prevention mode.
Nathan Goodyear

Docosahexaenoic Acid Reduces ER Stress and Abnormal Protein Accumulation and Improves N... - 0 views

    Animal study finds DHA aids recovery from TBI.
Nathan Goodyear

Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) - Nutrition and Traumatic Br... - 0 views

    Evidence does support that n-3 reduces inflammation; yet limited evidence exists to provide direct evidence that n-3 protects against TBI.
Nathan Goodyear

PLOS ONE: Depletion of Brain Docosahexaenoic Acid Impairs Recovery from Traumatic Brain... - 0 views

  • The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
  • LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
  • DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
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  • DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
  • DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
  • AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
  • Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
  • severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
  • Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
  • it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
  • severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
  • DHA deficiency further elevates TBI-induced production of SBDPs
  • less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
    mouse study finds prolonged recovery in DHA deficient mice compared to controls.
Nathan Goodyear

Neurobiological effects of the green tea constituent theanine and its potential role in... - 0 views

    Only abstract available: l-Theanine appears to be a glutamate receptor antagonist.  The effects of l-Theanine have shown to be positive with mood disorders, psychiatric conditions, and neurodegenerative diseases.  L-Theanine increases BDNF.
Nathan Goodyear

Diet-induced obesity and low testosterone increase neuroinflammation and impair neural ... - 0 views

  • both obesity and low testosterone are also risk factors for neural dysfunction, including cognitive impairment [] and development of AD
  • Levels of obesity and testosterone are often inversely correlated
  • diet-induced obesity causes significant metabolic disturbances and impairs central and peripheral nervous systems.
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  • both obesity and low testosterone are linked with promotion of inflammatory pathways [] and exert harmful actions on the central [] and peripheral [,] nervous systems
  • In general, obesity-related changes were worsened by low testosterone and improved by testosterone treatment; however, this relationship was not statistically significant in several instances. Further, our data suggest that a common pathway that may contribute to obesity and testosterone effects is regulation of inflammation
  • fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
  • testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
  • fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
  • testosterone status did not significantly affect body weight
  • testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
  • Prior work in rodents has shown diet-induced obesity induces insulin resistance in rat brain [] and that testosterone replacement improves insulin sensitivity in obese rats []. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [,] as well as obese men [], and (ii) androgen therapy can improve some metabolic measures in overweight men with low testosterone
  • it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
  • Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
  • Testosterone status also affected metabolic and neural measures
  • many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
  • neuroprotection [,], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
  • testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [] and neuroprotective [] actions
  • glia are the primary sources of proinflammatory molecules in the CNS
  • poorer survival of neurons grown on glia from mice maintained on high-fat diet
  • Since testosterone can affect glial function [] and improve neuronal growth and survival [], it was unexpected that testosterone status exhibited rather modest effects on neural health indices with the only significant response being an increase in survival in the testosterone-treated, high-fat diet group
  • significantly increased expression of TNFα and IL-1β in glia cultures derived from obese mice
  • testosterone treatment significantly lowered TNFα and IL-1β expression to near basal levels even in obese mice, indicating a protective benefit of testosterone across diet conditions
  • IL-1β treatment has been shown to induce synapse loss and inhibit differentiation of neurons
  • Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
  • testosterone prevented and/or restored thermal nociception in both diet groups
  • a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
    Study points to obesity and low Testosterone contribution of neuroinflammation.  No effect of body weight was seen with TRT.  This animal model found similar positive effects of TRT in insulin sensitivity.  Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line.  Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol.  Testosterone's effect on glial survival was positive but not significant.  Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta.   Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.
Nathan Goodyear

Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain an... - 0 views

    Only abstract available here, but sugar in the form of sucrose found to lower cortisol.  Increased activity in the hippocampus was evident in the sucrose arm of this study.  Both of these activities will lead to stress induced food addictions--particularly of sugar.  Sugar is highly addictive and should be especially avoided in children.  Of note, this study followed the cortisol levels through saliva.
Nathan Goodyear

Estrogen and brain-derived neurotrophic factor (BDNF) in hippocampus: complexity of ste... - 0 views

    Estrogen effects in the hippocampus with BDNF (surprise, surprise) appear to have different effects between the sexes.
Nathan Goodyear

What Happens to Your Brain on Sugar, Explained by Science - Mic - 0 views

    This is your brain on drugs, sorry I meant sugar.
Nathan Goodyear

BMC Neuroscience | Full text | The effect of adolescent testosterone on hippocampal BDN... - 0 views

    study finds that BDNF is more associated with cell proliferation and neurogenesis with normal circulating Testosterone levels.  
Nathan Goodyear

An inverse relationship between cortisol and BDNF levels in schizophrenia: data from hu... - 0 views

    Elevated Cortisol found to have inverse association with BDNF.
Nathan Goodyear

Lower low density lipid cholesterol levels are associated with Parkinson's disease - 0 views

    Lower LDL levels associated with increased risk of Parkinson's disease.  LDL levels < 113 were associated with a 3.5 fold increase in Parkinson's disease compared to LDL of 138.
Nathan Goodyear

Effects of testosterone administration on cognitive function in hys... - PubMed - NCBI - 0 views

    Testosterone therapy in women post-hysterectomy, with low total and low free Testosterone, provides no benefit in cognitive function.
Nathan Goodyear

Effects of the FITKids Randomized Controlled Trial on Executive Control and Brain Function - 0 views

    After school fitness/exercise improved focus, attention, and cognition of children.
Nathan Goodyear

Slow CCL2-dependent translocation of biopersistent particles from muscle to brain - 0 views

    Study finds translocation of alum from vaccines from muscle to brain in some individuals.  This leads to the neurologically condition termed Macrophagic myofasciitis.  Study after study has shown this connection and now studies are showing this translocation of immune cells to the brain resulting in neuro-inflammation.  All I hear from pro vaccinators is vitriol.  Here is science.
Nathan Goodyear

Thyroid hormone treated astrocytes induce maturation of cerebral cortical neurons throu... - 0 views

    T3 plays a significant role in astrocyte maturation.  This has significant cognitive and disease impact.
Nathan Goodyear

Nerve growth factor receptor immunoreactivit... [Mech Ageing Dev. 1993] - PubMed - NCBI - 0 views

    alpha-GPC appears to increase nerve growth factor receptors in rat brains. 
Nathan Goodyear

Behavioral effects of L-alpha-glycer... [Pharmacol Biochem Behav. 1992] - PubMed - NCBI - 0 views

    animal study finds improvement in learning and memory with alpha-GPC after 20 days of therapy.
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