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Archive - Feb 2, 2012


Alzheimer’s Disease May Spread by “Jumping” from One Brain Region to Another

For decades, researchers have debated whether Alzheimer’s disease starts independently in vulnerable brain regions at different times, or if it begins in one region and then spreads to neuroanatomically connected areas. A new study by Columbia University Medical Center (CUMC) researchers strongly supports the latter, demonstrating that abnormal tau protein, a key feature of the neurofibrillary tangles seen in the brains of those with Alzheimer’s, propagates along linked brain circuits, “jumping” from neuron to neuron. The findings, published February 1, 2012 in the online journal PloS One, open new opportunities for gaining a greater understanding of Alzheimer’s disease and other neurological diseases and for developing therapies to halt its progression, according to senior author Dr. Karen E. Duff, professor of pathology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute. Alzheimer’s disease, the most common form of dementia, is characterized by the accumulation of plaques (composed of amyloid-beta protein) and fibrous tangles (composed of abnormal tau protein) in brain cells called neurons. Postmortem studies of human brains and neuroimaging studies have suggested that the disease, especially the neurofibrillary tangle pathology, begins in the entorhinal cortex, which plays a key role in memory. Then, as Alzheimer’s progresses, the disease appears in anatomically linked higher brain regions. “Earlier research, including functional MRI studies in humans, have also supported this pattern of spread,” said study coauthor Dr. Scott A. Small, professor of neurology in the Sergievsky Center and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at CUMC.

Potential New Treatment for Leishmaniasis

Researchers at the University of Dundee in the UK have identified fexinidazole as a possible, much-needed, new treatment for the parasitic disease visceral leishmaniasis. Leishmaniasis is named after William Leishman, a Glasgwegian doctor who served with the British Army in India, and who first identified the parasite in the early 1900s. The disease is the second biggest killer in Africa, Asia, and Latin America after malaria, and affects 500,000 people, killing about 50,000-60,000 patients per year. Current drug treatments for the disease are unsatisfactory for reasons such as high cost, drug resistance, or the need for hospitalization. The disease is caused by the bite of a sand fly. Fexinidazole is already in phase 1 clinical trials for a related disease - African sleeping sickness – but a research team at Dundee, including Dr. Susan Wyllie, Professor Alan Fairlamb, and colleagues, has identified it as having potential in treating leishmaniasis. Their research was published February 1, 2012 in Science Translational Medicine, and was funded by the Wellcome Trust. Tests in mice showed that the drug has a greater than 98% rate of suppressing infection of leishmaniasis, comparable to current treatments such as miltefosine and Pentostam. These and other existing treatment options all suffer from disadvantages; they are not always safe, effective, or easy to administer. The only oral drug, miltefosine, cannot be given to women of child-bearing age due to a substantial risk of birth defects; other drugs are costly and have to be given by injection. Thus, there is a continuing need for safe and cost-effective drugs suitable for use in resource-poor settings. Professor Fairlamb said that fexinidazole has the potential to become a safe and effective oral drug therapy for treating the severest form of visceral leishmaniasis.