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etanercept in alzheimer

Yingjie Qi, Igor Klyubin, A Claudio Cuello, Michael J Rowan
Pro-inflammatory mechanisms have recently emerged as an important component of early Alzheimer's disease (AD) pathogenesis. A particularly attractive therapeutic strategy is to selectively prevent the disruptive effects of activation of the innate immune system in the brain at an early transitional stage by reducing the production or directly neutralizing pro-inflammatory cytokines, in particular IL-1β and TNF-α. Here we tested their in vivo effects on synaptic plasticity deficits, which provide sensitive and robust measures of synaptic failure, in a rat model of AD amyloidosis...
June 2018: Neurobiology of Disease
Daniah Shamim, Michael Laskowski
Tumor necrosis factor α (TNF-α) inhibitors have long been used as disease-modifying agents in immune disorders. Recently, research has shown a role of chronic neuroinflammation in the pathophysiology of neurodegenerative diseases such as Alzheimer disease, and interest has been generated in the use of anti-TNF agents and TNF-modulating agents for prevention and treatment. This article extensively reviewed literature on animal studies testing these agents. The results showed a role for direct and indirect TNF-α inhibition through agents such as thalidomide, 3,6-dithiothalidomide, etanercept, infliximab, exendin-4, sodium hydrosulfide, minocycline, imipramine, and atorvastatin...
2017: Journal of Central Nervous System Disease
Rudy Chang, Jillian Knox, Jae Chang, Aram Derbedrossian, Vitaly Vasilevko, David Cribbs, Ruben J Boado, William M Pardridge, Rachita K Sumbria
Tumor necrosis factor alpha (TNF-α) driven processes are involved at multiple stages of Alzheimer's disease (AD) pathophysiology and disease progression. Biologic TNF-α inhibitors (TNFIs) are the most potent class of TNFIs but cannot be developed for AD since these macromolecules do not cross the blood-brain barrier (BBB). A BBB-penetrating TNFI was engineered by the fusion of the extracellular domain of the type II human TNF receptor (TNFR) to a chimeric monoclonal antibody (mAb) against the mouse transferrin receptor (TfR), designated as the cTfRMAb-TNFR fusion protein...
July 3, 2017: Molecular Pharmaceutics
Abhijit Dey, Raktim Bhattacharya, Anuradha Mukherjee, Devendra Kumar Pandey
Alzheimer's disease (AD) is a severe, chronic and progressive neurodegenerative disease associated with memory and cognition impairment ultimately leading to death. It is the commonest reason of dementia in elderly populations mostly affecting beyond the age of 65. The pathogenesis is indicated by accumulation of the amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFT) in brain tissues and hyperphosphorylation of tau protein in neurons. The main cause is considered to be the formation of reactive oxygen species (ROS) due to oxidative stress...
March 2017: Biotechnology Advances
Richard C Chou, Michael Kane, Sanjay Ghimire, Shiva Gautam, Jiang Gui
INTRODUCTION: It is increasingly becoming accepted that inflammation may play an important role in the pathogenesis of Alzheimer's disease (AD), as several immune-related genes have been associated with AD. Among these is tumor necrosis factor (TNF)-α, a proinflammatory cytokine known to play an important role in autoimmune disorders, including rheumatoid arthritis (RA). Although AD and RA appear to involve similar pathological mechanisms through the production of TNF-α, the relationship between AD and RA remains unknown...
November 2016: CNS Drugs
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No abstract text is available yet for this article.
December 8, 2015: Neurology
Ayse N Tufan, Fatih Tufan
No abstract text is available yet for this article.
December 8, 2015: Neurology
Megan E Roerink, Rob Jm Groen, Gerben Franssen, Bianca Lemmers-van de Weem, Otto C Boerman, Jos Wm van der Meer
INTRODUCTION: Alzheimer's disease is a debilitating condition, and the search for an effective treatment is ongoing. Inflammation, in reaction to amyloid deposition, is thought to accelerate cognitive decline. With tumor necrosis factor α being an important proinflammatory cytokine, a recent trial investigated the effect of the tumor necrosis factor α inhibitor etanercept after peripheral administration in patients with Alzheimer's disease. Although there was no significant effect, others have claimed spectacular effects of etanercept after perispinal injection...
2015: Alzheimer's Research & Therapy
Joseph Butchart, Laura Brook, Vivienne Hopkins, Jessica Teeling, Ursula Püntener, David Culliford, Richard Sharples, Saif Sharif, Brady McFarlane, Rachel Raybould, Rhodri Thomas, Peter Passmore, V Hugh Perry, Clive Holmes
OBJECTIVES: To determine whether the tumor necrosis factor α inhibitor etanercept is well tolerated and obtain preliminary data on its safety in Alzheimer disease dementia. METHODS: In a double-blind study, patients with mild to moderate Alzheimer disease dementia were randomized (1:1) to subcutaneous etanercept (50 mg) once weekly or identical placebo over a 24-week period. Tolerability and safety of this medication was recorded including secondary outcomes of cognition, global function, behavior, and systemic cytokine levels at baseline, 12 weeks, 24 weeks, and following a 4-week washout period...
May 26, 2015: Neurology
H Kübra Elçioğlu, Levent Kabasakal, Fatih Tufan, Ömer H Elçioğlu, Seyhun Solakoglu, Tugba Kotil, Mehmet Akif Karan
Tumor necrosis factor-alpha (TNF-α) upregulation enhances amyloid β (Aβ) induced neurotoxicity in Alzheimer's disease (AD). Intracerebroventricular streptozotocin (STZ) administration causes pathological changes and cognitive deficits similar to those seen in AD by causing impairment of brain glucose and energy metabolism. Recent reports indicate a protective role of Thalidomide, Etanercept, and Infliximab, all of which have anti-TNF-α activity, against cognitive and neuropathological changes in experimental and clinical studies...
March 2015: Acta Histochemica
Edward Tobinick
Excess tumor necrosis factor (TNF) plays a pivotal role in the pathogenesis of Alzheimer's disease(AD). Clinical improvement following perispinal administration of etanercept in patients with Alzheimer's disease and other forms of dementia and brain dysfunction is characteristically evident within minutes. The rapidity and constellation of the clinical effects across multiple domains (cognition, mood, memory, motor function, and attention) suggest they are mediated by non-synaptic signaling mechanisms previously unrecognized for etanercept...
January 2012: Current Alzheimer Research
Catherine H Trepanier, Norton W Milgram
Alzheimer's disease (AD) is currently treated with cholinergic and glutamatergic therapies, which provide symptomatic benefit but do not reverse the underlying pathology or cognitive deficits. The prevalence of AD is expected to triple over the next 50 years, creating an urgency to develop effective "disease-modifying" therapies to reduce the economic burden of this devastating disorder. One of the main areas of therapeutic focus has been an antiinflammatory strategy based on an inflammatory hypothesis of AD...
2010: Journal of Alzheimer's Disease: JAD
Edward Tobinick
BACKGROUND: Thrombolytic therapy reduces stroke size and disability by reperfusion and salvage of ischaemic penumbra. Emerging evidence suggests that retrieved penumbra may be the site of ongoing inflammatory pathology that includes extensive microglial activation. Microglial activation may be associated with excessive levels of tumour necrosis factor (TNF) and resultant neurotoxicity. Etanercept, a potent biologic TNF antagonist, reduces microglial activation in experimental models and has been therapeutically effective in models of brain and neuronal injury...
February 2011: CNS Drugs
Keith A Wollen
Alzheimer's disease (AD) is characterized by dysfunctional intracellular and extracellular biochemical processes that result in neuron death. This article summarizes hypotheses regarding cell dysfunction in AD and discusses the effectiveness of, and problems with, different therapies. Pharmaceutical therapies discussed include cholinesterase inhibitors, memantine, antihypertensive drugs, anti-inflammatory drugs, secretase inhibitors, insulin resistance drugs, etanercept, brain-derived neurotrophic factor, and immunization...
September 2010: Alternative Medicine Review: a Journal of Clinical Therapeutic
Pamela E Potter
Development of effective treatments for patients with Alzheimer disease has been challenging. Currently approved treatments include acetylcholinesterase inhibitors and the N-methyl-D-aspartate receptor antagonist memantine hydrochloride. To investigate treatments in development for patients with Alzheimer disease, the author conducted a review of the literature. New approaches for treatment or prevention focus on several general areas, including cholinergic receptor agonists, drugs to decrease β-amyloid and tau levels, antiinflammatory agents, drugs to increase nitric oxide and cyclic guanosine monophosphate levels, and substances to reduce cell death or promote cellular regeneration...
September 2010: Journal of the American Osteopathic Association
L Fioravanzo, M Venturini, R Di Liddo, R D Liddo, F Marchi, C Grandi, P P Parnigotto, M Folin
Although Alzheimer's disease (AD) is considered a neurodengenerative disorders, in the last few years a large amount of evidence has suggested that it is also a vascular pathology characterized by increased capillary density and expression of angiogenic factors. In AD the endothelium degenerates, promoting local neuroinflammation and activation of brain endothelium, perivascular microglia, pericytes, astrocytes. Excess tumor necrosis factor (TNF) in the cerebrospinal fluid (CSF), at a concentration of 25 times higher than in the control group, has been demonstrated in AD...
November 2010: Current Alzheimer Research
Elisa Bassi, Claudia De Filippi
A 53-year-old woman with a history of psoriasis presented with severe cutaneous lesions associated with psoriasis. The woman was mentally handicapped; she was able to converse monosyllabically with her mother only and was very limited in social interactions. After preliminary investigations, a biological treatment was proposed. Etanercept was started in October 2006. The patient responded rapidly and, after 3 months, achieved a 75% improvement in the psoriasis area and severity index (PASI 75) score. Most notable, however, was that she began interacting with other people, even if they were not familiar to her...
2010: American Journal of Clinical Dermatology
Edward Tobinick
Etanercept is a potent antagonist of TNF, a pleotropic immune signaling molecule that is also a pivotal regulator of synaptic function. Excess TNF is centrally involved in the pathogenesis of a variety of inflammatory neurological disorders, including Alzheimer's disease, sciatica, traumatic brain injury and spinal cord injury. Perispinal etanercept produces rapid improvement in both Alzheimer's disease and sciatica and in other forms of disc-related pain. Basic research and the observed clinical effects suggest that etanercept has the surprising ability to penetrate into the cerebrospinal fluid after perispinal administration...
June 2010: Expert Review of Neurotherapeutics
Martin Soubrier, Stéphane Haïk, Jean-Jacques Hauw, Jean Christophe Corvol, Olivier Lyon-Caen, Maxime Dougados
We describe a patient in whom sporadic Creutzfeldt-Jakob disease (sCJD) occurred one year after the onset of etanercept therapy for rheumatoid arthritis (RA). This association could be a chance occurrence. However, TNF-alpha has been implicated in the pathogenesis of neurodegeneration in sCJD and etanercept might worsen the disease. Such an aggravation has been observed in multiple sclerosis, in which TNF-alpha is the key mediator of demyelination. It may be of interest studying the impact of treatment with TNF-alpha antagonists on prevalence and incidence of those neurodegenerative diseases involving TNF-alpha mediation, such as Alzheimer disease...
March 2010: Joint, Bone, Spine: Revue du Rhumatisme
Chittaranjan Andrade, Rajiv Radhakrishnan
The prevention and treatment of cognitive impairment in the elderly has assumed increasing importance in an aging population. This article presents a qualitative review of recent research on experimental interventions for the prevention and treatment of mild cognitive impairment and Alzheimer's disease in elderly subjects. Interventions addressed range from lifestyle measures to pharmacological treatments. Epidemiological studies suggest that dietary measures, physical exercise, and mental activity may reduce the risk of cognitive impairment and Alzheimer's disease in elderly subjects...
January 2009: Indian Journal of Psychiatry
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