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  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1186/s13024-017-0150-7.

Title:
NADPH oxidase in brain injury and neurodegenerative disorders | Molecular Neurodegeneration
Description:
Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {šŸ’ø}

We can't tell how the site generates income.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {šŸ”}

pubmed, nox, google, scholar, article, cas, nadph, oxidase, central, brain, oxidative, role, disease, injury, activation, mice, stress, studies, cell, ros, inhibition, expression, superoxide, cells, cerebral, neurodegenerative, increased, biol, stroke, sclerosis, activity, pphox, model, apocynin, damage, human, reported, microglia, zhang, shown, models, oxygen, inhibitor, disorders, ischemia, res, reactive, production, med, pathology,

Topics {āœ’ļø}

platelet-derived growth factor-induced n-methyl-d-aspartate receptors ubiquitin-proteosomal system-mediated degradation tumor necrosis factor-alpha ozone-induced airway hyperresponsiveness enhances tgf-β-induced apoptosis placebo-controlled double-blind study growth factor-induced production article download pdf hd140q/140q derived neurons angiotensin ii-induced hypertrophy castro-faria-neto hc enhancing pro-angiogenic signaling double-edged sword revisited aptamer-targeted oligonucleotide theranostics post-mortem brain tissue human platelet-rich plasma flavin adenine dinucleotide calcium-induced cell death il-13-induced oxidative stress signaling adaptor mal/tirap ageing-related neurodegenerative diseases surgically-induced brain injury head-tilt mice result neural stem/progenitor cells ortho-methoxy-substituted catechols nadph oxidase-mediated activation nadph oxidase-derived superoxide nadph oxidase-dependent signaling early nestin-expressing progenitors de silva tm podocyte-specific nadph oxidase 6-hydroxy-dopamine-induced neurodegeneration pi3k/akt-dependant manner blood–brain barrier dysfunction cd95-dependent hepatocyte apoptosis nonsteroidal anti-inflammatory drugs glucose-induced oxidative stress blood–brain barrier damage central nervous system anti-inflammatory microglial activation lps-induced animal model microglial/macrophage polarization dynamics single-stranded nucleic acids angiotensin ii-induced hypertension rna aptamer-based therapeutics nox1-dependent nadph oxidase reactive oxygen species-studies targeting microglia-mediated neurotoxicity increased nadph-oxidase activity

Questions {ā“}

  • A role for NOX NADPH oxidases in Alzheimer's disease and other types of dementia?
  • Glial cells and inflammation in Parkinson's disease: a role in neurodegeneration?
  • Is modulation of oxidative stress an answer?
  • Multiple sclerosis: an immune or neurodegenerative disorder?
  • NADPH oxidase inhibitors: new antihypertensive agents?
  • Which NADPH oxidase isoform is relevant for ischemic stroke?

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:NADPH oxidase in brain injury and neurodegenerative disorders
         description:Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.
         datePublished:2017-01-17T00:00:00Z
         dateModified:2017-01-17T00:00:00Z
         pageStart:1
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            Alzheimer’s disease
            Stroke
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            Parkinson’s disease
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            Molecular Medicine
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ScholarlyArticle:
      headline:NADPH oxidase in brain injury and neurodegenerative disorders
      description:Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.
      datePublished:2017-01-17T00:00:00Z
      dateModified:2017-01-17T00:00:00Z
      pageStart:1
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         Alzheimer’s disease
         Stroke
         Neurodegeneration
         Oxidative stress
         Traumatic brain injury
         Parkinson’s disease
         Amyotrophic lateral sclerosis
         Huntington’s disease
         Multiple sclerosis
         Neurosciences
         Neurology
         Molecular Medicine
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            address:
               name:Charlie Norwood VA Medical Center, Augusta, USA
               type:PostalAddress
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               type:PostalAddress
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               type:PostalAddress
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               type:PostalAddress
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      name:Ratna K. Vadlamudi
      affiliation:
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            address:
               name:Department of Obstetrics and Gynecology, University of Texas Health Science Center, San Antonio, USA
               type:PostalAddress
            type:Organization
      name:Darrell W. Brann
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            name:Charlie Norwood VA Medical Center
            address:
               name:Charlie Norwood VA Medical Center, Augusta, USA
               type:PostalAddress
            type:Organization
            name:Medical College of Georgia
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               name:Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta, USA
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PostalAddress:
      name:Charlie Norwood VA Medical Center, Augusta, USA
      name:Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta, USA
      name:Charlie Norwood VA Medical Center, Augusta, USA
      name:Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta, USA
      name:Charlie Norwood VA Medical Center, Augusta, USA
      name:Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta, USA
      name:Charlie Norwood VA Medical Center, Augusta, USA
      name:Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta, USA
      name:Charlie Norwood VA Medical Center, Augusta, USA
      name:Department of Neurosurgery, Medical College of Georgia, Augusta University, Augusta, USA
      name:Department of Obstetrics and Gynecology, University of Texas Health Science Center, San Antonio, USA
      name:Charlie Norwood VA Medical Center, Augusta, USA
      name:Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta, USA

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