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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

1α,25-dihydroxyvitamin D_{3} Interacts with Curcuminoids to Stimulate Amyloid... - 0 views

iospress.metapress.com/...k457101686r62685

curcumin vitamin D Beta-amyloid protein beta-amyloid Alzheimer's disease alzheimer

shared by Nathan Goodyear on 17 Sep 13 - No Cached
  • Nathan Goodyear on 17 Sep 13
     
    curcumin and vitamin D synergistic in beta-amyloid removal in Alzheimer's disease. 
Nathan Goodyear

Coconut oil attenuates the effects of amylo... [J Alzheimers Dis. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24150106

coconut oil coconut oil alzheimers mitochondria amyloid-beta

shared by Nathan Goodyear on 04 Jun 14 - No Cached
  • Nathan Goodyear on 04 Jun 14
     
    Coconut oil found to "rescue" neurons in vitro exposed to amyloid Beta.  It was also found to reduce/protect against mitochondrial damage from amyloid-beta.
Nathan Goodyear

Olive Component Oleuropein Promotes β-Cell Insulin Secretion and Protects β-C... - 0 views

pubs.acs.org/...acs.biochem.7b00199

olive oil diabetes metabolism insulin Oleuropein

shared by Nathan Goodyear on 18 Sep 17 - No Cached
  • Nathan Goodyear on 18 Sep 17
     
    Only abstract available here.  Study finds oleuropein, compound in olive oil, increases insulin secretion in response to glucose via unregulated ERK/MAPK signaling.  Oleuropein also blocked the cytotoxicity induced by amyloids i.e. beta amyloid plaques are well known hallmarks of Alzheimer's disease.
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
Nathan Goodyear

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!
Nathan Goodyear

Progesterone enhances transthyretin expressio... [J Mol Neurosci. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20535645

progesterone Alzheimer's disease alzheimer's disease Alzheimers Transthyretin hormone hormones postmenopause women menopause

shared by Nathan Goodyear on 17 Mar 14 - No Cached
  • Nathan Goodyear on 17 Mar 14
     
    Postmenopausal cognitive decline is a common complaint.  Declining Estradiol and progesterone have been implicated, in part, to this cognitive decline.  This study finds that progesterone increases expression of Transthyretin, a protein that processes amyloid Beta protein.  This amyloid Beta protein is associated with damage found in Alzheimer's. 
Nathan Goodyear

Decreased Accumulation of Subcellular Amyloid-β with Improved Mitochondrial F... - 0 views

iospress.metapress.com/...jp517wt324588874

Huperzine-A Huperzine Alzheimer's alzheimer's disease Alzheimers dementia mitochondria Beta-amyloid protein

shared by Nathan Goodyear on 09 Apr 14 - No Cached
  • Nathan Goodyear on 09 Apr 14
     
    Huperzine A, a natural acetylcholinesterase inhibitor, provides neuroprotection through increase mitochondrial function and decrease in accumulated amyloid Beta protein.
Nathan Goodyear

Genomic and Nongenomic Signaling Induced by 1α,25(OH)2-Vitamin D3 Promotes th... - 0 views

iospress.metapress.com/...1321517j461377p2

vitamin D amyloid plaque alzheimer's disease Alzheimer's disease brain

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • Nathan Goodyear on 01 Nov 13
     
    Vitamin D3 clears amyloid plaque from the brains of those battling Alzheimer's disease.
Nathan Goodyear

Insulin increases CSF Abeta42 levels in normal old... [Neurology. 2003] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12821730

insulin resistance IR brain neurology Beta-amyloid protein Alzheimer's disease

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    elevated insulin, found in insulin resistance, associated with disordered Beta-amyloid metabolism.
Nathan Goodyear

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.
Nathan Goodyear

Omega Research - 0 views

www.omega-research.com/researchview.php

omega-3 alzheimer's disease amyloid oxidative stress

shared by Nathan Goodyear on 15 Dec 10 - No Cached
  • Nathan Goodyear on 15 Dec 10
     
    omega-3 limit amyloid and oxidative damage; thus may decrease alzheimer's disease risk
Nathan Goodyear

A novel perspective for Alzheimer's disease... [J Alzheimers Dis. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20966550

alzheimer disease alzheimers amyloid-beta vitamin D vitamin d VDR receptor

shared by Nathan Goodyear on 04 Jun 14 - No Cached
  • Nathan Goodyear on 04 Jun 14
     
    Alzheimer's model finds that amyloid-beta supresses vitamin D receptor.  This study found that vitamin D therapy protected neurons by up regulating vitamin D receptors.  This prevented cytotoxicity and cell death.
Nathan Goodyear

Fish consumption among healthy adults is associated with decreased levels of inflammato... - 0 views

www.ncbi.nlm.nih.gov/...15992645

fish omega-3 omega 3 CRP IL-6 TNF-alpha amyloid WBC inflammation

shared by Nathan Goodyear on 14 Sep 17 - No Cached
  • Nathan Goodyear on 14 Sep 17
     
    Only abstract available here but higher fish intake associated with a decrease in CRP, IL-6, TNF-alpha, amyloid A and WBC; restated, higher fish intake associated with a reduction of inflammation
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

S-adenosylmethionine reduces the progress of... [Neurobiol Aging. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22221883

SAMe Alzheimer's disease Alzheimer's aging

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe helps to correct disordered homocysteine metabolism due to B- vitamin deficiency found in Alzheimer's disease.  SAMe show to reduce amyloid production, improve memory, decrease Tau, and reduced plaque formation.  Now, this was in a mice model, but SAMe as a methyl donor can benefit clients with dementia with minimal side effects.
Nathan Goodyear

Inflammatory Mechanisms in Alzheimer's Disease: Inhibition of β-Amyloid-Stimu... - 0 views

www.jneurosci.org/...558.full

microglia microglial cells inflammation Alzheimer's disease neurodegenerative

shared by Nathan Goodyear on 06 Jan 12 - No Cached
  • The activated microglia mount a complex local proinflammatory response
  • PPARγ plays a critical role in regulating the inflammatory responses of microglia and monocytes to β-amyloid
  • Nathan Goodyear on 06 Jan 12
     
    microglial and inflammatory response in Alzheimer's disease.  Agonists of PPAR-gamma inhibit this action.  This has important implications in reducing the local inflammatory response found in the brains of those with Alzheimers and other neuordegenerative disease.
Nathan Goodyear

Alzheimer's disease--synergistic effects of ... [J Neural Transm. 1998] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9720973

AD AGE advanced glycation end products Alzheimer's disease neurofibrillary tangles Beta-amyloid protein microglia brain neurology oxidative stress alzheimer

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • AGEs are protein modifications that contribute to the formation of the histopathological and biochemical hallmarks of AD: amyloid plaques, neurofibrillary tangles and activated microglia
  • Nathan Goodyear on 11 Jun 12
     
    good review of understanding of how poor glucose control, oxidative stress result in AGE and Alzheimer's disease.
Nathan Goodyear

Inflammatory Mechanisms in Alzheimer's Disease: Inhibition of β-Amyloid-Stimu... - 0 views

www.jneurosci.org/...558.long

inflammation AD alzheimer's neurodegenerative disease PPAR-gamma PPAR microglial alzheimer

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • PPARγ agonists were shown to inhibit the β-amyloid-stimulated expression of the cytokine genes interleukin-6 and tumor necrosis factor α. Furthermore, PPARγ agonists inhibited the expression of cyclooxygenase-2.
  • Nathan Goodyear on 11 Jun 12
     
    Not that we are recommending NSAIDS to reduce inflammation: but the learned biochemical pathways of inflammation involved with AD, allows a natural approach to reduce microglial associated inflammation through PPAR-gamma activation.
Nathan Goodyear

One year follow-up study of the association between chemical castration, sex hormones, ... - 0 views

www.sciencedirect.com/...S0306453003002208

hormone hormones depression memory beta-amyloid Testosterone Estradiol

shared by Nathan Goodyear on 03 Feb 14 - No Cached
  • Nathan Goodyear on 03 Feb 14
     
    Chemical castration as seen in androgen deprivation therapy resulted in precipitous decline in Testosterone and Estradiol in men.  Associated increased in beta-amylloid found.
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