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Nathan Goodyear

Increased neurogenesis and the ectopic granule cells after intrahippocampal BDNF infusi... - 0 views

www.sciencedirect.com/...S0014488604004431

BDNF brain derived neurotrophic factor hippocampus memory neuroplasticity

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    BDNF promotes neurogenesis in the hippocampus.  BDNF promotes neuroplasticity.
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

Fructose decreases physical activity and increases body fat without affecting hippocamp... - 0 views

www.nature.com/...srep09589.html

fructose obesity fat diet nutrition activity physical activity

shared by Nathan Goodyear on 03 Aug 15 - No Cached
  • the fructose animals gained significantly more weight than the glucose animals
  • The average liver mass of mice in the fructose treatment group was 20% heavier than for mice in the glucose group
  • The fat pads of mice consuming the fructose diet were 69% heavier than the fat pads of animals consuming the glucose diet
  • ...12 more annotations...
  • there are many studies showing that consumption of fructose in comparison to other monosaccharides results in increased de novo lipogenesis, dyslipidemia, insulin resistance, BW6, 7 and, most recently, impaired cognitive function
  • in the present study, the intake of fructose by mice was more similar to that of typical human consumption in comparison to previous studies
  • prolonged consumption of diets containing fructose (11 weeks) increased BW and body fat deposition
  • studies in humans confirm that fructose, but not glucose (when provided as 25% of energy requirements), in the context of an energy-balanced diet increases de novo lipogenesis and visceral adiposity along with dyslipidemia, decreases insulin sensitivity10, 12 and decreases in fat oxidation
  • we hypothesize that fructose may reduce voluntary energy expenditure in terms of physical activity.
  • significant reduction (~20%) in physical activity in the fructose-fed animals in comparison to glucose
  • a recent study reported that ingestion of fructose (25% energy intake, 10 weeks) in human volunteers also resulted in reduced energy expenditure in relation to a diet with the same glucose dose
  • There is certainly evidence to suggest that, for example, exercise is able to prevent dyslipidemia in healthy subjects fed a weight-maintenance high-fructose diet (30%)54, which strongly suggests a protective role of physical activity in metabolic regulation.
  • the potential negative effects of fructose in brain and cognitive function have been investigated, with a series of studies showing cognitive deficits in spatial memory and learning in adolescent and adult animals following access to a high fructose diet
  • access to both fructose and sucrose, but not glucose, results in a 40% reduction in hippocampal neurogenesis
  • Collectively these studies seem to suggest that fructose consumption can have a considerable impact on hippocampal function and learning, which is in direct contrast with what we observed.
  • the impact of fructose is apparent only in BW, liver mass and body fat, but not in cognitive measures or rates of neurogenesis
  • Nathan Goodyear on 03 Aug 15
     
    animal study finds that fructose increased liver mass, abdominal fat and decreased physical activity when compared to glucose.  The study groups were iso caloric, but one group was fed 18% fructose and the other 18% glucose.
Nathan Goodyear

Occupational mercury exposure and its consequences... [Int Arch Occup Environ Health. 1... - 0 views

www.ncbi.nlm.nih.gov/...7129652

mercury exposure occupational cognitive function memory behaviour

shared by Nathan Goodyear on 22 Feb 11 - No Cached
  • Mercury is a known neurotoxin
  • Nathan Goodyear on 22 Feb 11
     
    inorganic effects of mercury on behaviour and cognitive function
Nathan Goodyear

Effects of a standardized Bacopa monnieri extract ... [J Altern Complement Med. 2008] -... - 0 views

www.ncbi.nlm.nih.gov/...18611150

Bacopa elderly cognition memory natural therapy herb herbs

shared by Nathan Goodyear on 23 Aug 11 - No Cached
  • Nathan Goodyear on 23 Aug 11
     
    bacopa improves cognitive performance in elderly
Nathan Goodyear

Testosterone Treatment of Men With Mild Cognitive Impairment and Lo... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25392187

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shared by Nathan Goodyear on 24 Nov 14 - No Cached
  • Nathan Goodyear on 24 Nov 14
     
    small study finds limited improvement in cognition in men with low T and mild Cognitive impairment.  Little application from this study.
Nathan Goodyear

Estradiol concentrations and workin... [Psychoneuroendocrinology. 2013] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24011502

Estradiol E2 cognition hormone hormones women memory

shared by Nathan Goodyear on 06 Aug 14 - No Cached
  • Nathan Goodyear on 06 Aug 14
     
    women with high E2 versus low E2 had better cognitive function.
Nathan Goodyear

Exercise Induces Hippocampal BDNF through a PGC-1α/FNDC5 Pathway: Cell Metabo... - 0 views

www.cell.com/...S1550-4131(13)00377-X

brain memory focus attention learning exercise BDNF brain derived neurotrophic factor PGC-1alpha irisin FNDC5 hippocampus cognition

shared by Nathan Goodyear on 12 Aug 14 - No Cached
  • Nathan Goodyear on 12 Aug 14
     
    Brain benefits of exercise explained.  Exercise increases hippocampal BDNF via PGC-1alpha from skeletal muscle.
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...25430996

Testosterone women female hormone hormones menopause brain cognition memory hysterectomy

shared by Nathan Goodyear on 02 Dec 14 - No Cached
  • Nathan Goodyear on 02 Dec 14
     
    Testosterone therapy in women post-hysterectomy, with low total and low free Testosterone, provides no benefit in cognitive function.
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shared by wheelchairindia9 on 24 Feb 16 - No Cached
  • wheelchairindia9 on 24 Feb 16
     
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www.wheelchairindia.com/...Cervical-Pillow-Deluxe

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shared by wheelchairindia9 on 24 Feb 16 - No Cached
  • wheelchairindia9 on 24 Feb 16
     
    Cervical Pillow Deluxe will give you maximum comfort and support, regardless of which position you sleep in. Relieves muscle tension, stress and strain. Improves sleeping posture. Comfortable & protective support. Cervical Pillow Deluxe Features Orthopaedic Cervical Neck Pillow will give you maximum comfort and support, regardless of which position you sleep in. Relieves muscle tension, stress and strain. Improves sleeping posture. Comfortable and protective support.
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.
  • ...45 more annotations...
  • 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

Modifiable Risk Factors and Brain Positron Emission Tomography Measures of Amyloid and ... - 0 views

www.ajgponline.org/...fulltext

nutrition exercise mediterranean diet BMI weight alzheimer's disease brain

shared by Nathan Goodyear on 22 Aug 16 - No Cached
  • Nathan Goodyear on 22 Aug 16
     
    Can Alzheimer's be prevented?  New study suggests that nutrition, exercise, and healthy weight are key to Alzheimer's prevention.  A decrease in amyloid plaques and tau tangles were noted in normal BMI individuals, those with greater physical activity and those on a mediterranean diet.
Nathan Goodyear

Immune responses to malignancies - 0 views

www.ncbi.nlm.nih.gov/...PMC3721350

cancer immune system

shared by Nathan Goodyear on 18 Apr 18 - No Cached
  • increased densities of T-cell infiltrates with a high proportion of CD8+ T cells within primary colorectal carcinomas were associated with a significant protection against tumor recurrence
  • coexpression of genes mediating cytotoxicity and TH1 adaptive immune responses accurately predicted survival in patients with colorectal carcinoma independently of the metastatic status.
  • tumor-specific cytolytic T lymphocytes (CTLs)
  • ...10 more annotations...
  • tumor-associated antigens (TAs)
  • Proinflammatory cytokines secreted by inflammatory cells can contribute to tumor progression, and soluble factors produced by the tumor in response to nonspecific or tumor-specific signals, such as prostaglandin E2 (PGE2), adenosine, or TGF-β, downregulate functions of immune cells
  • they are largely ineffective in arresting tumor growth, although they can proliferate and mediate antitumor cytotoxicity on their removal from the tumor bed and ex vivo IL-2 activation.42
  • DCs (HLA-DR+CD86+CD80+CD14−) are nature’s best APCs
  • They are a common component of tumor immune infiltrates and are responsible for the uptake, processing, and cross-presentation of TAs to naive or memory T cells, thus playing a crucial role in the generation of tumor-specific effector T cells
  • DCs control the induction of Treg cells. In patients with cancer, cellular interactions between antigen-presenting DCs and T cells lead to expansion and accumulation of Treg cells at the tumor site and in the periphery
  • NK cells (CD3−CD56+CD16+), which mediate innate immunity and contain both perforin-rich and granzyme-rich granules, are well equipped to mediate lysis of tumor cells
  • B cells (CD19+, CD20+) are also rare in most human tumors, with the exception of breast cancer and melanoma
  • The initial acute inflammation involving the recruitment and influx of antitumor effector cells is replaced by chronic inflammation in later stages of tumor progression
  • Tissue hypoxia plays a major role in shaping the nature of immune infiltrates in tumors
  • Nathan Goodyear on 18 Apr 18
     
    Another great review of the immune system during different stages of carcinogenesis; how the cancer manipulates the immue system to cloak itself from the immune system.
Nathan Goodyear

Frontiers | Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of... - 0 views

journal.frontiersin.org/...full

LPS lipopolysaccharides Alzheimer's disease brain inflammation

shared by Nathan Goodyear on 23 Sep 17 - No Cached
  • lipopolysaccharides (LPS), either alone or in combination, have indicated that when compared, bacterial LPSs exhibit the strongest induction of pro-inflammatory signaling in human neuronal–glial cells in primary coculture of any single inducer, and different LPS extracts from different gastrointestinal (GI)-tract resident Gram-negative bacteria appeared to have different pro-inflammatory potential
  • powerful inducer of the NF-κB
  • In both neocortex and hippocampus, LPS has been detected to range from a ~7- to ~21-fold increase abundance in AD brain
  • ...15 more annotations...
  • Major Gram-negative bacilli of the human GI-tract, such as the abundant B. fragilis and Escherichia coli (E. coli), are capable of discharging a remarkably complex assortment of pro-inflammatory neurotoxins
  • (i) bacterial amyloids (10, 21); (ii) endotoxins and exotoxins (5, 12); (iii) LPS (12, 18); and (iv) small non-coding RNAs (sncRNAs)
  • integral components of the outer leaflet of the outer membrane of Gram-negative bacteria, LPS
  • LPS, the major molecular component of the outer membrane of Gram-negative bacteria normally serves as a physical barrier providing the bacteria protection from its surroundings
  • LPS is also recognized by the immune system as a marker for the detection of bacterial pathogen invasion and responsible for the development of inflammatory response is perhaps the most potent stimulator and trigger of inflammation known
  • AD-affected brains have remarkably large loads of bacterial-derived toxins compared to controls. The transfer of noxious, pro-inflammatory molecules from the GI-tract microbiome to the CNS may be increasingly important during the course of aging when both the GI-tract and blood–brain barriers become significantly more permeable
  • first evidence of a perinuclear association of LPS with AD brain cell nuclei
  • LPS-mediated stimulation of chronic inflammation, beta-amyloid accumulation, and episodic memory decline in murine models of AD (39, 40) and a biophysical association of LPS with amyloid deposits and blood vessels in human AD patients
  • Strong adherence of LPS to the nuclear periphery has recently been shown to inhibit nuclear maturation and function that may impair or block export of mRNA signals from brain cell nuclei, a highly active organelle with extremely high rates of transcription, mRNA processing, and export into the cytoplasm
  • LPS may be further injurious to the nuclear membrane just as LPS contributes to cerebrovascular endothelial cell membrane injury
  • high intake of dietary fiber is a strong inhibitor of B. fragilis abundance and proliferation in the intact human GI-tract and as such is a potent inhibitor of the neurotoxic B. fragilis-derived amyloids, LPS, enterotoxins, and sncRNAs.
  • GI-tract microbiome-derived LPS may be an important initiator and/or significant contributor to inflammatory degeneration in the AD CNS
  • LPS has been recently localized to the same anatomical regions involved in AD-type neuropathology
  • a known pro-inflammatory transcription factor complex that triggers the expression of pathogenic pathways involved in neurodegenerative inflammation
  • pro-inflammatory amyloids, endo- and exotoxins, LPSs, and sncRNAs but also serve as potent sources of membrane-disrupting agents
  • Nathan Goodyear on 23 Sep 17
     
    LPS links gut to inflammation in Alzheimer's disease
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