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Alzheimer's study first to explain death of brain cells
March 15, 2006Study is giant leap towards prevention and treatment
Researchers at Children's Hospital & Research Center at Oakland (CHRCO) have published a new study that is the first to explain how brain cells die in patients with Alzheimer's Disease. This discovery is an important first step to helping researchers devise ways to slow, prevent and eventually cure a disease that affects an estimated 4.5 million Americans.
In a study published in the February 28th issue of the Proceedings of the National Academy of Sciences, lead scientist Hani Atamna, Ph.D., found that alterations in the production of heme (a molecule that contains iron) may be the key to understanding why excessive amyloid-beta is toxic to brain cells. Dr. Atamna had previously discovered that Alzheimer's patients have abnormal amounts of heme in their brains. In new research results, Atamna's team showed that amyloid-beta readily binds with heme to form a compound that can be flushed from cells. When there is insufficient heme or too much amyloid-beta, however, the amyloid-beta forms large toxic "clumps" that the cell cannot dissolve and eliminate.
Though heme binding with amyloid-beta can be beneficial, if too much heme is bound up with amyloid-beta, there may be insufficient heme available for the cell to properly function. When this happens, the cell's mitochondria, which are the tiny structures inside brain cells that produce the energy the cells need to function, begin to decay. Dr. Atamna refers to this phenomenon as a "functional heme deficiency" because the cells are still forming heme, but it is trapped within an amyloid-beta/heme compound.
When they examined the heme/ amyloid-beta compound researchers in the Atamna laboratory were surprised to discover it was a peroxidase-a type of enzyme that reacts harmfully with biological materials essential for proper brain function such as serotonin and L-DOPA. Dr. Atamna believes that the combination of functional heme deficiency, which harms mitochondria needed to produce energy, together with the increase in oxidative damage caused by the peroxidase, is what eventually kills the cell.
"Until now, we didn't understand all the factors that trigger Alzheimer's disease. The discovery of the formation of amyloid-beta peroxidase provides a clear picture of why cells die in the brain of Alzheimer's patients. Our next challenge is to develop drugs that directly and selectively target the excessive peroxidase of amyloid-beta, which could lead to the first significant therapy for Alzheimer's disease."
Children's Hospital & Research Center at Oakland
Though heme binding with amyloid-beta can be beneficial, if too much heme is bound up with amyloid-beta, there may be insufficient heme available for the cell to properly function. When this happens, the cell's mitochondria, which are the tiny structures inside brain cells that produce the energy the cells need to function, begin to decay. Dr. Atamna refers to this phenomenon as a "functional heme deficiency" because the cells are still forming heme, but it is trapped within an amyloid-beta/heme compound.
When they examined the heme/ amyloid-beta compound researchers in the Atamna laboratory were surprised to discover it was a peroxidase-a type of enzyme that reacts harmfully with biological materials essential for proper brain function such as serotonin and L-DOPA. Dr. Atamna believes that the combination of functional heme deficiency, which harms mitochondria needed to produce energy, together with the increase in oxidative damage caused by the peroxidase, is what eventually kills the cell.
"Until now, we didn't understand all the factors that trigger Alzheimer's disease. The discovery of the formation of amyloid-beta peroxidase provides a clear picture of why cells die in the brain of Alzheimer's patients. Our next challenge is to develop drugs that directly and selectively target the excessive peroxidase of amyloid-beta, which could lead to the first significant therapy for Alzheimer's disease."
Children's Hospital & Research Center at Oakland
Brain Cells Current Events and Brain Cells News RSSResearch reveals lipids' unexpected role in triggering death of brain cells
The lipid that accumulates in brain cells of individuals with an inherited enzyme disorder also drives the cell death that is a hallmark of the disease, according to new research led by St. Jude Children's Research Hospital investigators.
Novel mouse gene reduces major pathologies associated with Alzheimer's disease
A new study reveals that a previously undiscovered mouse gene reduces the two major pathological perturbations commonly associated with Alzheimer's disease (AD).
Mouse gene suppresses Alzheimer's plaques and tangles
Investigators at Burnham Institute for Medical Research (Burnham) and colleagues have identified a novel mouse gene (Rps23r1) that reduces the accumulation of two toxic proteins that are major players in Alzheimer's disease: amyloid beta and tau.
Estrogen therapy likely must be given soon after menopause to provide stroke protection
For estrogen replacement to provide stroke protection, it likely must be given soon after levels drop because of menopause or surgical removal of the ovaries, scientists report in the Journal of Neuroscience.
ISU researchers' findings bring hope for possible Parkinson's disease cure
Researchers at Iowa State University have found an essential key to possibly cure Parkinson's disease and are looking for others.
Clinical tests begin on medication to correct Fragile X defect
NIH-supported scientists at Seaside Therapeutics in Cambridge, Mass., are beginning a clinical trial of a potential medication designed to correct a central neurochemical defect underlying Fragile X syndrome, the most common inherited cause of intellectual disability.
Mobile microscopes illuminate the brain
The majority of our life is spent moving around a static world and we generate our impression of the world using visual and other senses simultaneously.
This is your brain on fatty acids
Saturated fats have a deservedly bad reputation, but Johns Hopkins scientists have discovered that a sticky lipid occurring naturally at high levels in the brain may help us memorize grandma's recipe for cinnamon buns, as well as recall how, decades ago, she served them up steaming from the oven.
Stress-induced changes in brain circuitry linked to cocaine relapse
Stress-evoked changes in circuits that regulate serotonin in certain parts of the brain can precipitate a low mood and a relapse in cocaine-seeking, based on mouse studies published online this week in the Proceedings of the National Academy of Sciences.
Member of NFL Hall of Fame diagnosed with degenerative brain disease
The Center for the Study of Traumatic Encephalopathy (CSTE) at Boston University School of Medicine (BUSM) announced today that a recently deceased member of the NFL Hall of Fame suffered from the degenerative brain disease Chronic Traumatic Encephalopathy (CTE) when he died, becoming the 10th former NFL player diagnosed with the disease.
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