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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
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    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

MedLink - 0 views

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    Mercury exposure associated with polyneuropathy. Sensory is more recent exposure with long term exposure associated with motor.
Nathan Goodyear

Early repeated administration of progesterone improves the recovery of neuropathic pain... - 0 views

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    Very interesting article.  Early Progesterone treatment, in animal model, shown to improve neuropathic pain recovery.  This is by no means the first study to show this.  This has been shown numerous times in TBI, but the timing of therapy was the purpose of this article.  What is very interesting here is that the metabolites implicated here in the recovery are the same metabolites implicated in an increased tumor potential.
Nathan Goodyear

Toxic Effects of Mercury on the Cardiovascular and Central Nervous Systems - 0 views

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    Good review of the toxic effects of Hg on the CNS and cardiovascular system.
Nathan Goodyear

The molecular basis of neurodegeneration in multiple sclerosis - 0 views

  • Inflammation is the most predominant feature during the early (relaping) phases of the disease and declines with aging of the patients and disease duration
  • in the process of oligodendrocyte destruction and demyelination in MS lesions iron is liberated from its intracellular ferritin bound stores into the extracellular space, where it is taken up by microglia and macrophages and again stored together with ferritin. When this happens in MS lesions in an environment, where free radicals are produced by oxidative burst, iron can be liberated from ferritin and transformed into reactive Fe++[114], which reacts with hydrogen peroxide to generate highly reactive hydroxyl radicals [36] and thus amplifies oxidative damage and associated cellular injury
  • anti-inflammatory or immunomodulatory treatments are effective in the relapsing stage, but the benefit is lost when the patients have entered the progressive phase
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  • Inflammation will remain a key target, since the data suggest that microglia activation and oxidative burst is driven by inflammation throughout all stages of the disease.
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    Very nice review of the neurodegenerative process in MS.  
Nathan Goodyear

Vitamin D in the healthy and inflamed central nervous system: access and function - 0 views

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    Vitamin D3 helpful in treatment of an inflamed CNS, such as in TBI, MS...Vitamin D protects against the development of MS and the progression of MS.
Nathan Goodyear

Membrane Estrogen Receptors Stimulate Intracellular Calcium Release and Progesterone Sy... - 0 views

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    Estradiol stimulates hypothalamic progesterone synthesis in astrocytes in rat model.  This occurs through activation of calcium channels and influx of calcium.  ER alpha appears to be the prominent ER involved.
Nathan Goodyear

Central nervous system disease in patients with macrop... [Brain. 2001] - PubMed - NCBI - 0 views

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    Macrophagic myofasciitis and CNS disease. This study describes disease that mimics MS as a result of aluminum.
Nathan Goodyear

Lead exposure, polymorphisms in genes related to oxidative stress and risk of adult bra... - 0 views

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    another study that showed that lead exposure in susceptible individuals increased risk of CNS tumors, including menngiomas, and gliomas.  The apparent mechanism in this study was proposed through oxidative damage.  
Nathan Goodyear

Lead, Genetic Susceptibility, and Risk of Adult Brain Tumors - 0 views

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    this study suggests that Pb exposure, in those with ALAD polymorphism, have an increased risk of meningioma.
Nathan Goodyear

Understanding the Direct Synaptic Effects of Estradiol - 0 views

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    commentary on the current state of knowledge of estrogen receptors, particularily ER alpha, and brain synapsis.
Nathan Goodyear

International Journal of Obesity - Late-life obesity is associated with smaller global ... - 0 views

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    Need your brain at its peak performance?  Better lose weight if you are overweight.  Studies show a reduced brain volume and decreased cognitive function in those that are overweight.
Nathan Goodyear

ScienceDirect.com - Frontiers in Neuroendocrinology - Progesterone receptors: Form and ... - 0 views

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    progesterone through progesterone receptors, shown to have protective, anti-inflammatory effects in the CNS.
Nathan Goodyear

Oxidative stress and neurodegeneration: where are we now? - Halliwell - 2006 - Journal ... - 0 views

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    Fantastic review of oxidative damage and the CNS.  This is a 2006 review of our understanding of how neurodegeneration occurs through oxidative stress and of course poor detoxification.
Nathan Goodyear

A radical approach to stroke therapy - 0 views

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    vitamin C shown to benefit stroke patients.  Vitamin C, ascorbic acid, is extremely prevalent in the brain.  Functions to scavenge free radicals
Nathan Goodyear

Central Nervous system control of food intake - 0 views

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    For you biochemistry junkies. A great review of how the Gut and CNS communicate to regulate food intake
Nathan Goodyear

Progesterone exerts neuroprotective effects after brain injury 10.1016/j.brainresrev.20... - 0 views

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    progesterone shown to have neuroprotective and  healing properties in the CNS.  This has implications in Stroke, and possibly even excitotoxic disease such as Parkinson's, Alzhemier's...
Nathan Goodyear

Activation of CNS Inflammatory Pathways by Interferon-alpha: Relationship to Monoamines... - 0 views

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    mechanism of peripheral inflammation , via IFN-alpha and IL-6, contribution to depression
Nathan Goodyear

Access : Central nervous system control of food intake : Nature - 0 views

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    great review on CNS regulation of food intake
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