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Nathan Goodyear

JAMA Network | Archives of Neurology | Damage to Lipids, Proteins, DNA, and RNA in Mild... - 0 views

archneur.jamanetwork.com/article.aspx

neurodegenerative disease free-radicals Alzheimer's disease Alzheimer's oxidative stress oxidative damage lipid peroxides isoprostanes 8-hydroxy-2-deoxyguanosine neurology

shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    oxidative damage found to be present in early Alzheimer's disease.  This early mild cognitive impairment is the time for treatment to delay disease progression.  As this study points out, most studies up to this point have been done on individuals with late Alzheimer's disease.  This show that oxidative damage plays a prominent role in disease development.  This study found oxidative damage through several markers: lipid peroxides,isoprostanes, 8-hydroxy-2-deoxyguanosine...
Nathan Goodyear

Targeting Synaptic Dysfunction in Alzheimer's Disease by Administering a Specific Nutri... - 0 views

iospress.metapress.com/...gg33167h46757165

alzheimer's disease Alzheimer's disease DHA EPA Folate B12 B6 vitamin E C vitamins brain

shared by Nathan Goodyear on 04 Dec 13 - No Cached
  • Nathan Goodyear on 04 Dec 13
     
    Combination of DHA, EPA, choline, phospholipids, Folate, B12, B6, vitamin C and E, and selenium improves memory and cognitive function in those with mild Alzheimer's disease.
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

Androgen Deprivation Therapy and Future Alzheimer's Disease Risk - 0 views

jco.ascopubs.org/...JCO.2015.63.6266

ADT androgen deprivation therapy low T low Testosterone alzheimer's disease Alzheimer's brain

shared by Nathan Goodyear on 30 Dec 15 - No Cached
  • Nathan Goodyear on 30 Dec 15
     
    Androgen deprivation therapy appears to increase Alzheimer's disease risk.  In this study, the men on ADT the longest was found to be associated with increased diagnosis of Alzheimer's disease.
Nathan Goodyear

Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimer's disease - 0 views

www.chinaphar.com/...391.pdf

Huperzine-A memory cognition Alzheimer's Alzheimer's disease acetylcholinesterase inhibitor

shared by Nathan Goodyear on 03 Oct 12 - No Cached
  • Nathan Goodyear on 03 Oct 12
     
    small study, but well designed that showed that huperzine A supplementation improved executive function in Alzheimer's patients. Huperzine A is an acetylcholinesterase inhibitor.
Nathan Goodyear

Huperzine A for Alzheimer's disease. [Cochrane Database Syst Rev. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18425924

alzheimer disease Alzheimer's disease Alzheimer's Huperzine-A memory cognition

shared by Nathan Goodyear on 03 Oct 12 - No Cached
  • Nathan Goodyear on 03 Oct 12
     
    Review of 6 trials on 454 patients found Huperzine A improved cognition and executive function with no serious adverse events in patients with Alzheimer's disease.  Yet, their conclusion is, "...inadequate evidence to make any recommendation..."   Does it improve executive cognitive function?   Yes.  Does in have serious side effects?  No.  And we are waiting on...?
Nathan Goodyear

Effect of supplementation of vi... [J Nutr Sci Vitaminol (Tokyo). 2001] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...11814146

vitamin C ascorbic acid Alzheimer's disease acetylcholine memory

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    vitamin C inhibits acetylcholinesterase.  This will increase acetylcholine and thus can play a role in Alzheimer's disease.  People with Alzheimers disease have low levels of Vitamin C.  Vitamin C shown to improve memory in Alzheimer's mouse model.
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

Huperzine A in the Treatment of Alzheimer's Disease and Vascular Dementia: A Meta-Analysis - 0 views

www.hindawi.com/...363985

dementia Alzheimer's alzheimer's disease alzheimer disease huperzine A

shared by Nathan Goodyear on 30 Sep 14 - No Cached
  • Nathan Goodyear on 30 Sep 14
     
    Good review of the data on Huperzine A and Alzheimer's dementia.
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

Lipid-Based Diets Improve Muscarinic Neurotransmission in the Hippocampus of Transgenic... - 0 views

www.eurekaselect.com/...article

lipids fat high fat diet ketogenic diet brain alzheimer's disease brain health nutrition

shared by Nathan Goodyear on 15 Feb 16 - No Cached
  • Nathan Goodyear on 15 Feb 16
     
    Proof of concept study in Alzheimer's model finds high fat diet improves brain cholinergic synapses, targeting directly the neurotransmission deficits in Alzheimer's disease
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

Huperzine a as potential treatment of Alzheim... [Chem Biodivers. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21766442

Huperzine-A Alzheimer's disease Alzheimer's

shared by Nathan Goodyear on 03 Oct 12 - No Cached
  • Nathan Goodyear on 03 Oct 12
     
    Huperzine A at doses up to 400 mcg shown to benefit people with Alzheimer's disease, with no significant side effects.
Nathan Goodyear

Using Multicountry Ecological and Observational Studies to Determine Dietary Risk Facto... - 0 views

www.tandfonline.com/...07315724.2016.1161566

alzheimer's disease Alzheimers nutrition diet western diet

shared by Nathan Goodyear on 29 Aug 16 - No Cached
  • Nathan Goodyear on 29 Aug 16
     
    Western diet appears to be major risk association/factor in Alzheimer's disease risk.
Nathan Goodyear

Access : Blockade of the KATP channel Kir6.2 by memantine represents a novel mechanism ... - 0 views

www.nature.com/...mp2016187a.html

alzheimer's disease Alzheimer's brain insulin diabetes disease

shared by Nathan Goodyear on 02 Dec 16 - No Cached
  • Nathan Goodyear on 02 Dec 16
     
    Study of memantine finds effect on insulin is the same in the brain as in the pancreas.  In essence, Alzheimer's disease, is in part, a diabetes of the brain disease.
Nathan Goodyear

Calcium: A target in the war on Alzheimer's disease - 0 views

dl-web.dropbox.com/...heimers_Disease_WhitePaper.pdf

Alzheimer's disease excitotoxicity neurotoxicity calcium

shared by Nathan Goodyear on 17 Feb 12 - No Cached
  • Nathan Goodyear on 17 Feb 12
     
    good discussion on Alzheimer's disease and the role of calcium
Nathan Goodyear

Ketone bodies as a therapeutic for Alzheim... [Neurotherapeutics. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18625458

ketone bodies ketosis Alzheimer's disease Alzheimer's neurodegenerative disease

shared by Nathan Goodyear on 25 Jun 12 - No Cached
  • Nathan Goodyear on 25 Jun 12
     
    Ketone bodies have been shown to benefit the mitochondria in the brains of those with Alzheimer's disease.  This ketosis can be achieved through low carb/protein, high fat 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

S-adenosylmethionine prevents oxidative str... [J Alzheimers Dis. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20413874

SAMe Alzheimer's disease Alzheimer's

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe shown to be neuroprotective by increasing SOD activity, increasing glutathione production and decreasing homocysteine levels in Alzheimer's even in the presence of vitamin B deficiency.
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.
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