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Researchers report that oligomers of A?, released by ?-secretase activity, drive cell cycle re-entry…

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Clinical testing of a new, innovative method to treat Alzheimer’s disease began in March 2008 at Karolinska University Hospital, Stockholm. (See press release from April 7, 2008: http://www.karolinska.se/Pressmeddelanden). Six patients have now received brain implants of small capsules containing protein-producing cells.

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Patients with fibromyalgia may have perfusion abnormalities in the brain associated with pain processing, according to the results of a small study published in the November issue of the Journal of Nuclear Medicine.

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Many women may have sexual problems, butthat doesn’t mean it bothers them.

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HealthDay - MONDAY, Nov. 3 (HealthDay News) — Having diabetes or high blood pressure may hasten the death of people with Alzheimer’s disease, new research suggests.

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They’re more than twice as likely to die sooner, study finds

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Scientists have discovered a crucial step in hormone-triggered bone growth, a finding that could lead to new osteoporosis drugs and better bone-building therapies, according to a new study. The research was performed at the University of Alabama at Birmingham (UAB). It showed that parathyroid hormone (PTH) given intermittently enhances the body’s own bone-building action through a specific “co-receptor” on the surface of bone cells.

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As the population ages and hospitals reach full capacity, integrating inpatient systems and telemedicine programs will be crucial. A recent forecast by analyst firm Datamonitor, London and New York, states that by 2012 the overall telehealth market should exceed $8 billion, up from $1.2 billion today.

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Abstract: Background: This work sought to determine the effects of hypothalamic proline-rich peptide (PRP)-1 in a rat model of Alzheimer’s disease.Methods: Complex histochemical, electrophysiologic, and behavioral analyses were performed on intact or diseased Wistar rats (n = 28). Pathologic conditions were induced by bilateral intracerebroventricular injection of amyloid peptide A?25–35. The diseased rats received systemic administration of PRP-1 or placebo control.Results: A?25–35 caused cellular neurodegeneration with marked glial reaction in the hippocampal complex and almost full destruction of the dentate fascia, which was not observed in conditions of PRP-1 administration after A?25–35 injection. Hippocampal neurons of intact animals responded to high-frequency (tetanic) stimulation of entorhinal cortex of ipsilateral cerebral hemisphere by tetanic and posttetanic potentiation of a different intensity and duration, which was accompanied by posttetanic depression. A?25–35 led to significant changes in the level and pattern of hippocampal neuronal activity, indicating the absence of both tetanic and posttetanic activity. Poststimulus activity manifestations rarely occurred and rapidly decreased after repeated trials. This indicated the focal character of lesion. Regular administration of PRP-1 for 4 weeks resulted in optimal restoration of electrophysiologic parameters. PRP-1 maintained the initial learning level achieved in a behavioral study in a Morris water maze.Conclusions: Systemic administration of PRP-1 possesses neuroprotective effects and can prevent the neurodegeneration in hippocampus induced by A?25–35. This suggests that PRP-1 could be a potential therapeutic agent for specific neurodegenerative diseases.

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