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New synthetic compounds appear to prevent brain cell death
December 21, 2005Spanish chemists have developed a promising set of synthetic compounds that one day could help slow or perhaps halt the progression of Alzheimer's disease and other neurological disorders. The preliminary finding, based on test tube studies by researchers at the Universidad de Granada and others, appears in the Dec. 29 issue of the American Chemical Society's Journal of Medicinal Chemistry.
The compounds, particularly a synthesized metabolite of the hormone melatonin, all inhibit an enzyme called inducible nitric oxide synthase (iNOS), which is needed to produce nitric oxide (NO). NO, a signaling molecule that can activate the immune system, plays an important role in the brain, according to the researchers. But too much NO can trigger the death of brain cells and some scientists theorize the compound is involved in the development of Alzheimer's and Parkinson's diseases.
Like melatonin, the new synthetic compounds apparently can cross biological barriers, suppress iNOS production, and, in turn, prevent NO-induced brain damage, the researchers say. However, they caution that additional research will be needed to verify these results.
The American Chemical Society - the world's largest scientific society - is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
American Chemical Society
The American Chemical Society - the world's largest scientific society - is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
American Chemical Society
Brain Cell Death Current Events and Brain Cell Death News RSSNew understanding about mechanism for cell death after stroke leads to possible therapy
Scientists at the Brain Research Centre, a partnership of the University of British Columbia Faculty of Medicine and Vancouver Coastal Health Research Institute, have uncovered new information about the mechanism by which brain cells die following a stroke, as well as a possible way to mitigate that damage.
Life and death in the living brain
Like clockwork, brain regions in many songbird species expand and shrink seasonally in response to hormones. Now, for the first time, University of Washington neurobiologists have interrupted this natural "annual remodeling" of the brain and have shown that there is a direct link between the death of old neurons and their replacement by newly born ones in a living vertebrate.
Popular Alzheimer's theory may be false trail
The idea that anti-inflammatory drugs might protect people struggling with dementia from Alzheimer's disease has received a blow with the online release of a study of human brain tissue in Acta Neuropathologica.
Drug's epilepsy-prevention effect may be widely applicable
A drug with potential to prevent epilepsy caused by a genetic condition may also help prevent more common forms of epilepsy caused by brain injury.
Alzheimer's: New findings resolve long dispute about how the disease might kill brain cells
For a decade, Alzheimer's disease researchers have been entrenched in debate about one of the mechanisms believed to be responsible for brain cell death and memory loss in the illness.
Slices of living brain tissue are helping scientists identify new stroke therapies
Slices of living human brain tissue are helping scientists learn which drugs can block the waves of death that engulf and engorge brain cells following a stroke.
Matrix fragments trigger fatal excitement
Shredded extracellular matrix (ECM) is toxic to neurons. Chen et al. reveal a new mechanism for how ECM demolition causes brain damage. The study will appear in the December 29, 2008 issue of The Journal of Cell Biology (www.jcb.org).
Common epilepsy drug could prevent and treat Alzheimer's disease
The team led by UBC Psychiatry Prof. Weihong Song, who is also the Jack Brown and Family Professor and Chair in Alzheimer's Disease at UBC, found that if Valproic Acid (VPA) is used as a treatment in early stages of AD memory deficit is reversed.
Scientists find a key culprit in stroke brain cell damage
Researchers have identified a key player in the killing of brain cells after a stroke or a seizure. The protein asparagine endopeptidase (AEP) unleashes enzymes that break down brain cells' DNA, scientists at Emory University School of Medicine have found.
Epilepsy-induced brain cell damage prevented in the laboratory
For some epilepsy patients, the side effects of epilepsy can be as troubling as the seizures. One pressing concern is the cognitive impairment seizures often inflict, which potentially includes memory loss, slowed reactions and reduced attention spans.
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Thomistic Principles and Bioethics (Routledge Annals of Bioethics) by Jason T. Eberl (Author) Thomas Aquinas is one of the foremost thinkers in Western philosophy and Christian scholarship, recognized as a significant voice in both theological discussions and secular philosophical debates. Alongside a revival of interest in Thomism in philosophy, scholars have realized its relevance when addressing certain contemporary issues in bioethics. This book offers a rigorous interpretation of Aquinas's metaphysics and ethical thought, and highlights its significance to questions in bioethics. Jason T. Eberl applies Aquinas's views on the seminal topics of human nature and morality to key questions in bioethics at the margins of human life - questions which are currently contested in the academia, politics and the media such as: ยท When does a human person's life begin? How should... |
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Brain Cells Blue Sky Black Death Feat. Virtuoso (Primary Contributor) |
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Where is God? Scientific Millennium Discovery of SPIRITUAL BRAIN CELLS by Richard L. Harding (Author) It appears God's job-prospectus is thousands of years old. Revolutionary changes are creating new questions never before asked by mankind, such as Where Is God? What does God look like? What about the newest scientific discovery of spiritual brain cells found in the frontal lobes of the forehead? What about death? etc. Please allow me to introduce a book that has been 68 years in the writing. After my first visit to a funeral home and then experiencing an end-of-the-world scenario over the radio as a youngster, my life has been a quest for the answer to one basic question, Where Is God? Religious fiction dominates the literary marketplace. But, God is not fiction, but fact. My journey into light has sought for real answers to settle the endless human issues of terrorism,... |
![Assessment of the effects of the cyclooxygenase-2 inhibitor rofecoxib on visuospatial learning and hippocampal cell death following kainate-induced seizures ... [An article from: Cognitive Brain Research]](http://ecx.images-amazon.com/images/I/51w5k0y0LAL._SL160_.jpg) |
Assessment of the effects of the cyclooxygenase-2 inhibitor rofecoxib on visuospatial learning and hippocampal cell death following kainate-induced seizures ... [An article from: Cognitive Brain Research] by T. Kunz (Author), N. Marklund (Author), L. Hillered (Author), E.H. Oliw (Author) This digital document is a journal article from Cognitive Brain Research, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser. Description: Kainate-induced seizures result in hippocampal neurodegeneration and spatial learning deficits in rodents. Previous studies show that rofecoxib, a selective cyclooxygenase-2 inhibitor, protects against kainate-induced hippocampal cell death 3 days after seizures. Our aim was to determine whether rofecoxib attenuates visuospatial learning deficits and late neuronal death after kainate-induced seizures. Seizures were induced in Sprague-Dawley rats with kainic acid (10 mg/kg, i.p.). Eight hours later, animals... |
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Stress, the Aging Brain, and the Mechanisms of Neuron Death (Bradford Books) by Robert M. Sapolsky (Author) Looking beyond the now widely recognized relationships between stress and physical illness, this accessible and engagingly written book suggests that stress and stress-related hormones can also endanger the brain. Strategies to reduce stress and methods to protect neurons from further damage are proposed, and the relevance for humans of the animal research findings are clearly delineated. Sapolsky provides an extensive review of the recent, exciting data on glucocorticoids, the adrenal steroid hormones (hydrocortisone or cortisol in humans) that are released during stress. Excessive exposure to these hormones can damage the brain and make neurons more vulnerable to neurological insults. The findings he reports and ideas he synthesizes may have profound implications for understanding... |
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