{"id":12582,"date":"2016-12-23T08:47:02","date_gmt":"2016-12-23T08:47:02","guid":{"rendered":"http:\/\/www.kurzweilai.net\/?p=291394"},"modified":"2016-12-28T10:24:41","modified_gmt":"2016-12-28T10:24:41","slug":"method-discovered-to-remove-damaging-amyloid-plaques-found-in-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/hoo.central12.com\/fugic\/2016\/12\/23\/method-discovered-to-remove-damaging-amyloid-plaques-found-in-alzheimers-disease\/","title":{"rendered":"Method discovered to remove damaging amyloid plaques found in Alzheimer’s disease"},"content":{"rendered":"
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Illustration of formation of beta-amyloid plaque. Enzymes act on the APP (amyloid precursor protein) and cut it into fragments. The beta-amyloid fragment is crucial in the formation of senile plaques in Alzheimer\u2019s disease. (credit: National Institute on Aging\/NIH)<\/p><\/div>\n

German scientists have discovered a strategy for removing amyloid<\/a> plaques — newly forming clumps in a brain with Alzheimer’s disease<\/a> that are created by misfolded proteins that clump together and damage nerve cells.<\/p>\n

The scientists from the German Center for Neurodegenerative Diseases (DZNE)<\/a> in Munich and the Ludwig Maximilians University (LMU) Munich<\/a> took aged\u00a0microglia cells (the\u00a0 scavenger cells of the brain’s immune system) from a mouse model of Alzheimer’s disease and co-cultured them with microglia tissue from younger mouse brains. Surprisingly, within a few days, they found that the older amyloid plaques started to rejuvenate, resume cell division, and clear the brain from plaques by engulfing them. The amyloid plaque clearance potential of aged\u00a0Alzheimer’s disease microglia could be fully restored, despite the continuous loss of neurons and astrocytes.<\/p>\n

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Cortical atrophy in Alzheimer’s Disease, associated with loss of gyri and sulci in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus (credit: Doctor Jana\/CC via Wikipedia)<\/p><\/div>\n

They also found that the young microglia cells were secreting factors that helped the old microglia rejuvenate — especially a protein called “granulocyte-macrophage colony stimulating factor<\/a>” (GM-CSF)* — which alone could do the job. Depletion of either old or young microglial cells prevented amyloid plaque clearance, indicating a synergistic effect of both populations.<\/p>\n

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Click the image to view a DZNE video that describes the role of dysfunctional proteins in creating amyloid plaque in early Alzheimer’s disease, starting at 2:25. (credit: DZNE)<\/p><\/div>\n

GM-CSF has previously been reported to reduce plaques and improve cognition in a mouse model of Alzheimer’s disease, but it’s not yet known if GM-CSF could potentially work as a new drug for Alzheimer’s disease in humans. Also, microglia secrete small proteins that induce inflammatory reactions and may harm neurons, the researchers say.<\/p>\n

The researchers suggest that the new model system can be explored further to search for additional factors that enhance the clearance of amyloid plaques.<\/p>\n

The work was published this week in\u00a0The EMBO Journal<\/em>.<\/p>\n