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Nathan Goodyear

Estrogen, neuroinflammation and neuroprotection... [Neuroscience. 2006] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...16337092

estrogen neuroinflammation inflammation Parkinson's disease women postmenopausal

shared by Nathan Goodyear on 14 Dec 11 - No Cached
  • Nathan Goodyear on 14 Dec 11
     
    Estrogen important in reducing neuroinflammation in Parkinson's disease in postmenopausal women?
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...PMC4190446

Testosterone neuroinflammation glia insulin resistance obesity diabetes brain CNS PNS inflammation low T low Testosterone TNF-alpha IL-1beta

shared by Nathan Goodyear on 28 Apr 15 - No Cached
  • both obesity and low testosterone are also risk factors for neural dysfunction, including cognitive impairment [58–61] 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.
  • ...23 more annotations...
  • both obesity and low testosterone are linked with promotion of inflammatory pathways [70–72] and exert harmful actions on the central [73–75] and peripheral [29,76] 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 [63] and that testosterone replacement improves insulin sensitivity in obese rats [64]. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [30,65] as well as obese men [66], 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 [80,81], 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 [82] and neuroprotective [83] 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 [86] and improve neuronal growth and survival [87–89], 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
  • Nathan Goodyear on 28 Apr 15
     
    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

IOS Press - Journal Article - 0 views

iospress.metapress.com/...vux3g01201610607

neuroinflammation excitotoxicity inflammation air pollution air pollution Alzheimer's disease IL-6 IL-1 TNF-alpha IFN-gamma

shared by Nathan Goodyear on 31 Jan 12 - No Cached
  • Nathan Goodyear on 31 Jan 12
     
    neuroinflammaiton, also described as excitotoxicity, found in the brains of children/young adults that lived in high air pollution areas.  Neuroinflammation (IL-6, IL-1, TNF-alpha, IFN-gamma...) found in the brains of these children and young adults.  This is the same process found in Alzheimers and other excitotoxicity disease states.  Addtionally, it is also involved in most chronic diseases of aging.
Nathan Goodyear

Diet-induced obesity and low testosteron... [J Neuroinflammation. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25224590

low T low Testosterone low T men male hormones hormone Testosterone diet indued obesity DIO alzheimer's disease diabetes obesity inflammation

shared by Nathan Goodyear on 17 Sep 14 - No Cached
  • Nathan Goodyear on 17 Sep 14
     
    animal model finds that low Testosterone and diet induced obesity leads to neuroinflammation and increased risk of Diabetes and Alzheimer's disease.
Nathan Goodyear

Mary Ann Liebert, Inc. - Journal of Neurotrauma - 0(ja): - 0 views

www.liebertonline.com/...neu.2011.1922

sulphoraphane Nrf2 glutathione inflammation neuroinflammation oxidative damage cytokines

shared by Nathan Goodyear on 24 Aug 11 - No Cached
  • Nathan Goodyear on 24 Aug 11
     
    sulphoraphane activates Nrf2 pathway, which promotes Glutathione production, plays role in reducing oxidative damage and neuroinflammation
Nathan Goodyear

Exogenous melatonin restrains neuroinflammation in high fat diet induced diabetic rats ... - 0 views

www.sciencedirect.com/...S0024320520301740

GSH inflammation IDO indoleamine dioxygenase glutathione melatonin

shared by Nathan Goodyear on 18 Nov 22 - No Cached
  • Nathan Goodyear on 18 Nov 22
     
    Melatonin as a downregulator of IDO and GSH in neuroinflammation.
Nathan Goodyear

Neuroinflammation in Parkinson's disease: a ta... [Lancet Neurol. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19296921

glial cells Parkinson's disease neurodegenerative disorders inflammation neuroinflammation

shared by Nathan Goodyear on 14 Dec 11 - No Cached
  • Nathan Goodyear on 14 Dec 11
     
    activated glial cells play important role in Parkinson's disease and other neuroimflammatory diseases
Nathan Goodyear

New Study Links Aluminum Adjuvants in Vaccines with Neurological Disorders | Health Imp... - 0 views

healthimpactnews.com/...es-with-neurological-disorders

aluminum vaccines vaccinations brain neurology inflammation Macrophagic myofasciitis Macrophagic myofasciitis

shared by Nathan Goodyear on 09 Oct 13 - No Cached
  • Nathan Goodyear on 09 Oct 13
     
    good review of the biochemistry of neuroinflammation and aluminum from Macrophagic myofasciitis.
Nathan Goodyear

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

www.issfal.org/...r-traumatic-injury-and-surgery

omega 3 omega-3 DHA EPA TBI memory cognition inflammation traumatic brain injury brain injury brain

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • Nathan Goodyear on 31 Aug 15
     
    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 Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

nnr.sagepub.com/...75.long

curcumin DHA TBI traumatic brain injury brain injury neuroinflammation BDNF brain derived neurotrophic factor brain

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • 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.
  • Nathan Goodyear on 31 Aug 15
     
    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

The kynurenine pathway and inflammation in amyotro... [Neurotox Res. 2010] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...19921535

kynurenine pathway inflammation neurodegenerative disease

shared by Nathan Goodyear on 12 Apr 11 - No Cached
  • We show the presence of neuroinflammation in ALS and provide the first strong evidence for the involvement of the KP in ALS. These data point to an inflammation-driven excitotoxic-chelation defective mechanism in ALS, which may be amenable to inhibitors of the KP
  • Nathan Goodyear on 12 Apr 11
     
    kynnurenine pathway, inflammation and neurodegenerative disease
Nathan Goodyear

Stuck at the bench: Potential natural neuroprotective compounds for concussion - 0 views

www.ncbi.nlm.nih.gov/...PMC3205506

concussions concussion natural therapies brain curcumin omega 3 resveratrol green tea EGCG EPA DHA vitamin E vitamin c vitamin D

shared by Nathan Goodyear on 20 Feb 16 - No Cached
  • Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
  • The predominant CNS polyunsaturated fatty acid is DHA
  • effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
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  • multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
  • pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
  • The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
  • DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
  • potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
  • Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
  • Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
  • Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
  • Clinical trials in Alzheimer's disease have also been largely ineffective
  • The clinical evidence thus far appears equivocal
  • curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
  • Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
  • in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
  • Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
  • studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
  • no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
  • studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
  • green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
  • At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
  • a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
  • Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
  • Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
  • potent anti-oxidant EGCG which is capable of crossing the blood-nerve and blood-brain barrier,
  • Epigallocatechin-3-gallate also displays neuroprotective properties
  • More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
  • Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
  • in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
  • Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
  • emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
  • high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
  • it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
  • one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
  • Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
  • Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
  • One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
  • These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
  • preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
  • Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
  • At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
  • patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
  • CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
  • Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
  • chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
  • Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
  • Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease
  • Nathan Goodyear on 20 Feb 16
     
    great review of natural therapies in the treatment of concussions
Nathan Goodyear

Exposure to the Functional Bacterial Amyloid Protein Curli Enhances Alpha-Synuclein Agg... - 0 views

www.nature.com/srep34477

neurodegenerative disease amyloid alzheimer's disease Parkinson's disease gut gut flora gut microbiome gut microbiota gut-brain

shared by Nathan Goodyear on 06 Oct 16 - No Cached
  • Our work suggests that protein misfolding and immune activation in neurodegenerative disorders are triggered through cross-seeding by exposure to exogenous microbial amyloids in the nose, mouth and gut.
  • Streptococcus mutans, Staphlococcus aureus, Salmonella enterica, Mycobacterium tuberculosis and others
  • Gene homologs encoding curli were recently determined also in four phyla: Bacteroidetes, Proteobacteria, Firmicutes, and Thermodesulfobacteria
  • ...8 more annotations...
  • changes in the gut microbiota induced by antibiotics alter neuroinflammation and amyloid deposition in a mouse model of AD
  • Our data suggest that amyloid proteins in the microbiota are involved in the origination and maintenance of neurodegenerative disease.
  • exposure to bacteria producing a functional extracellular amyloid protein enhances aggregation of AS in brain neurons in aged rats and in muscle cells in nematodes
  • AS aggregates seed aggregation of tau
  • involvement of the vagus nerve in PD
  • microgliosis, astrogliosis and enhanced expression of IL-6, TLR2 and TNF in the brain following curli exposure suggest the occurrence of an enhanced local sterile inflammatory response to AS in the brain.
  • the immune system in both AD and PD have now been extensively established
  • TLR2 activation through exposure to bacterial amyloid is pathogenic
  • Nathan Goodyear on 06 Oct 16
     
    Gut bacteria may play crucial role in systemic inflammation that leads to Alzheimer's and Parkinson's disease.  These amyloid production bacteria trigger systemic inflammation that leads to microglia activation and amyloid in the brain.   More establishment of the gut-brain connection.  
Nathan Goodyear

Cannabidiol reduces neuroinflammation and promotes neuroplasticity and functional recov... - 0 views

www.sciencedirect.com/...S0278584616302524

brain cod cannabinoids hemp oil BDNF neuroplasticity TBI brain injury

shared by Nathan Goodyear on 11 Aug 17 - No Cached
  • Nathan Goodyear on 11 Aug 17
     
    CBD increases BDNF--neuroplasticity.
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