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Activating stem cells may treat Alzheimer's
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     Stem cells offer promise in treating neurodegenerative diseases but not in the expected way, according to researchers at the annual symposium on dementia and Alzheimer抯 disease, sponsored by the Albert Einstein College of Medicine and Montefiore Medical Center in New York.

    Longevity genes might protect against Alzheimer抯 disease and combining drugs and non-pharmacological interventions might slow the disease. Researchers recommended a quick office test to identify patients with early dementia.

    Cases of dementia cases in the United States are expected to double in the next 40 years, said Gary Kennedy, professor of psychiatry and behavioral sciences at Einstein and director of geriatric psychiatry at Montefiore. Currently, Alzheimer抯 disease alone affects 8% to 15% of American citizens aged at least 65, he said. He added that modest interventions would help patients and care givers by postponing decline.

    Stem cells are present throughout the brain and, if doctors knew the signals, could be activated to repair injury due to stroke, trauma, multiple sclerosis, or neurodegenerative diseases, such as Alzheimer抯 disease, said Mark Mehler, chairman of the neurology department at Einstein. "Pharmacology is not selective. We need to understand the basic biology," he told the BMJ. Stem cells in the brain need to be activated within specific brain regions, where they have molecular signals to integrate them with other brain cells. Just transplanting stem cells into the brain and hoping they will work will not be effective, he said.

    Although the ability to activate stem cells in the brain was "years off," Dr Mehler told the BMJ that the drugs used in cancer chemotherapy may affect proteins altered in neurodegeneratives diseases. The interleukins, colony stimulating factors, and erythropoietin cross the blood-brain barrier, which becomes more porous in neurodegenerative disease, he said.

    Also speaking at the conference, Nir Barzilai, director of Einstein抯 institute of ageing research, reported that three genes may explain why only one in 10 000 people live to be 100. His study included more than 1200 people, 300 Ashkenazi Jews (Jews of Eastern European descent) aged 95 to 108, their spouses, and their children, many of whom have already lived beyond the US average lifespan.

    The CETP gene, which regulates lipoproteins, is found in about 8% of 65 year olds but in 25% of those who live to 105. Lipoproteins move cholesterol and triglycerides through the bloodstream and may increase high density lipoprotein, the "good cholesterol." People with the CETP gene have unusually large lipoprotein particles, but no one knows how this might be protective. People with this gene also have good cognitive function in old age. Two other genes, apoC-III and APM1, also seem connected to longer life, he said.

    Steven Hahn, professor of clinical medicine at Einstein and director of the primary care internal residency programme described a test for dementia that can be done in a primary care setting. About 75% of dementia is not recognised by outpatient providers, but the memory impairment screen is a convenient detection test.

    The patient is given a written list of four words and asked to read them aloud and remember them (the words history, factory, policeman, and toothbrush are often used). The person giving the test also tells the patient a cue for each category (for history, "something you might have studied in school").

    The test giver involves the patient in unrelated discussion for two minutes and then asks the patient to recall the words. Two points are scored for each word freely recalled and one point for each word recalled on cue. Scores of four or lower predict dementia with a sensitivity of 0.87 and a specificity of 0.96(Janice Hopkins Tanne)