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Risk factors for progression of brain atrophy in aging - 0 views

www.neurology.org/...1704.abstract HgbA1C brain volume glucose
shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    increasing HgbA1c associated decreasing brain volume in the elderly population.  This decrease in brain volume was found in asymptomatic individuals.  Take home:  poor blood glucose control and increasing glycation of hemoglobin results in brain loss.
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Does insulin dysfunction play a role in... [Trends Pharmacol Sci. 2002] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12084635 insulin insulin resistance Beta-amyloid protein tau proteins Alzheimer' brain neurologys disease AD free radicals
shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    elevated insulin levels associated with disordered Beta-amyloid metabolism and hyperphosphorylation of tau proteins.  Free radicals also play a role as well.
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High total cholesterol levels in late life associated with a reduced risk of dementia - 0 views

www.neurology.org/...1689.abstract cholesterol neurodegenerative disease dementia
shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    higher cholesterol levels associated with a decreased dementia risk in the elderly population.  Stop the press!!  Yes, basic physiology tells us this. The brain loves cholesterol, cholesterol is needed. The question is: what will be the impact of "neurodegenerative diseases" by the overzealous use of statins?
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Lymphocyte oxidative DNA damage and plasma antioxidants in Alzheimer Disease - 0 views

www.lycoredindia.com/...TI_18.pdf oxidative damage oxidative stress 8-hydroxy-2-deoxyguanosine free radicals Alzheimer's Alzheimer's disease neurology brain
shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    This study found an inverse association between elevated 8-hydroxy-2-deoxyguanosine and low antioxidants in individuals with Alzheimer's disease.
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Central obesity and the aging brain - 0 views

idealab.ucdavis.edu/...jagust_harvey_etal_AN2005.pdf obesity weight loss waist to hip ratio brain neurology hippocampus
shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    This study showed that abdominal obesity was associated with a smaller brain volume. Specifically, a high waist to hip ratio was associated with a 27% reduction in hippocampal volume.
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Neuronal membrane cholesterol loss enhances amyloid peptide generation - 0 views

jcb.rupress.org/953 cholesterol neurodegeneration neurodegenerative disease brain neurology Beta-amyloid protein Alzheimer's disease
shared by Nathan Goodyear on 14 Jun 12 - No Cached
  • Nathan Goodyear on 14 Jun 12
     
    low neuronal cholesterol increases risk of neurodegeneration.  Low Cholesterol in neurons increases B-amyloid protein formation.  Are we increasing Alzheimer's incidence by lowering cholesterol too much?  After all, the brain needs cholesterol!
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Dyslipidemia is a protective factor in amyotrophic lateral sclerosis - 0 views

www.neurology.org/...1004.short ALS amyotrophic lateral sclerosis LDL:HDL cholesterol neurodegenerative disease
shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Correlation studies demonstrated that bearing an abnormally elevated LDL/HDL ratio significantly increased survival by more than 12 months.
  • Nathan Goodyear on 13 Jun 12
     
    high LDL:HDL ratios in ALS patients, resulted in increased survival at 12 months.
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Cholesterol-lowering therapy and cell membranes. Stable plaque at the expense of unsta... - 0 views

www.lizscript.co.uk/...AMS01.pdf cholesterol neurology brain neurodegenerative disease statins statin therapy
shared by Nathan Goodyear on 21 Jun 12 - No Cached
  • Nathan Goodyear on 21 Jun 12
     
    This article tells it all in the conclusion: "Changing our current practice pattern could take many years, but we may one day prescribe cholesterol-raising medications to certain patients". The long term effect of lowering cholesterol MAY stabilize plaques (not reduce), but at the expense of the brain. So, we may all have stable plaques, but we just won't know it because our brains will be fried.
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Olive oil consumption, plasma oleic acid, and stroke incidence - 0 views

www.neurology.org/...WNL.0b013e318220abeb.abstract olive oil oleic acid stroke
shared by Nathan Goodyear on 21 Jun 12 - No Cached
  • Nathan Goodyear on 21 Jun 12
     
    Individuals with olive oil intake have lower risk of stroke.  41% and 73% lower!
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Better memory functioning associated with higher total and LDL cholesterol levels in ve... - 0 views

www.ncbi.nlm.nih.gov/...PMC2614555 cholesterol LDL brain neurology memory levels elderly
shared by Nathan Goodyear on 19 Jun 12 - No Cached
  • Nathan Goodyear on 19 Jun 12
     
    higher total cholesterol and LDL associated with better memory in the elderly population.  This was present in those without APOE4 allele
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High normal plasma triglycerides are associated with preserved cognitive function in Ch... - 1 views

ageing.oxfordjournals.org/...ageing.afs033.abstract triglyceride triglycerides cognitive function lipids neurology
shared by Nathan Goodyear on 19 Jun 12 - No Cached
  • Nathan Goodyear on 19 Jun 12
     
    Higher triglyceride levels associated with better cognitive function versus those with lower triglyceride levels in an elderly chinese population.
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Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172 metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation
shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
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In vitro neurotoxicity of methylisothiazolinone, ... [J Neurosci. 2002] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12196562 methylisothiazolinone MI neurotoxic neurology brain neurotoxicity
shared by Nathan Goodyear on 15 Jul 13 - No Cached
  • Nathan Goodyear on 15 Jul 13
     
    Scary.  Common component of many OTC creams and ointments contain chemical, methylisothiazolinone that is neurotoxic.
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Increased risk of cognitive impairment or dementia in women who underwent oophorectomy ... - 0 views

www.neurology.org/...1074 dementia cognitive decline menopause Estrogen women HRT HT BHRT hormone hormones
shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Nathan Goodyear on 06 Aug 13
     
    Untold risk of early ovary removal appears to be cognitive decline and increased risk of dementia.  The earlier the age of removal, the more the increased risk of cognitive decline.  
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Is Timing Everything? New Insights into Why the Effect of Estrogen Therapy on Memory Mi... - 0 views

endo.endojournals.org/...2570.full estrogen therapy memory hormone therapy HRT BHRT Estradiol neurology brain women hormone hormones
shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Women who have an oophorectomy before the normal age at menopause show an increased risk for cognitive impairment or dementia later in life unless they are treated with estrogen until the normal age at menopause
  • SIRT1 has been implicated in the disruption of mitochondrial bioenergenetics in Alzheimer's disease and mild cognitive impairment
  • the increase in dementia observed with CEE/MPA rather than CEE alone suggests potential deleterious effects of MPA on brain function in older women
  • ...1 more annotation...
  • SIRT 1 as a potential mediator of the impact of E2
  • Nathan Goodyear on 06 Aug 13
     
    Early estrogen therapy in perimenopause and early menopause, with Estradiol, provides more health benefits than later therapy.  This article looked at Estrogen's effects on a woman's brain.  This likely has its origins in the change in estrogen receptors. The signal is not changing, but the reception of that signal is.  How else can one explain a different response to the same hormone dosage?
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MicroRNAs in the Aging Female Brain: A Putative Mechanism for Age-Specific Estrogen Eff... - 0 views

endo.endojournals.org/...2795.abstract aging female brain estrogen HRT BHRT hormone hormones menopause neurology memory Estradiol
shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Nathan Goodyear on 06 Aug 13
     
    Estradiol appears to have an age dependent effect on the transcription of mRNA and brain neuroplasticity.  This has a future impact on the risk of cognitive decline and dementia in elderly women.  This is only the abstract, but points to one effect of early Estradiol effect on improved brain health versus late therapy.  
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The projected effect of risk factor reduction on Alzheimer's disease prevalence : The L... - 0 views

www.thelancet.com/...fulltext alzheimer's disease brain
shared by Nathan Goodyear on 12 Nov 13 - No Cached
  • Nathan Goodyear on 12 Nov 13
     
    Study suggests that >50% of cases of Alzheimer's can be prevented through lifestyle change.  
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Vitamin B supplementation, homocysteine levels, and the risk of cerebrovascular disease - 0 views

www.neurology.org/...WNL.0b013e3182a823cc.abstract B vitamins homocysteine stroke vitamins B CVA
shared by Nathan Goodyear on 30 Sep 13 - No Cached
  • Nathan Goodyear on 30 Sep 13
     
    B vitamin supplementation reduces homocysteine levels and risk of stroke.  This study only looked at B-12.  
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Unrecognized vitamin D3 deficiency is common in Parkinson disease - 0 views

www.neurology.org/...WNL.0b013e3182a95818.abstract vitamin d deficiency Parkinson's disease
shared by Nathan Goodyear on 30 Sep 13 - No Cached
  • Nathan Goodyear on 30 Sep 13
     
    low Vitamin D associated with Parkinson's disease
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Curcumin attenuates aluminum-induced oxidative ... [Neurotox Res. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21656326 curcumin oxidative stress inflammation mitochondria aluminum AL vaccine vaccination brain neurology
shared by Nathan Goodyear on 25 Nov 13 - No Cached
  • Nathan Goodyear on 25 Nov 13
     
    Curcumin shown to inhibit oxidative stress, inflammation, and mitochondrial damage caused by Aluminum in rat brain.  Aluminum's effect is not just confined to rat models.  It is well known to cause similar results in the human brain as well.  what is interesting about this article is the clear pathway disruption described as a result of Aluminum exposure.
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