Possible Improvement In Halting Alzheimer's Progression

Scientists May Have Just Discovered The Key To Halting Alzheimer's

Brain inflammation plays a big role in the disease's progression.

Caroline Gregoire | January 11, 2016 

Curbing brain inflammation may help people treat and prevent Alzheimer's disease, according to a landmark new study.
Researchers at the University of Southampton in England conducted a series of experiments showing a chemical that reduces neuroinflammation may have the potential to protect against the memory and behavioral changes associated with the disease that affects roughly 5.3 million Americans. 

"Quick Facts." Source: http://www.alz.org/facts/

<more at http://www.huffingtonpost.com/entry/brain-inflammation-alzheimers_568fff10e4b0a2b6fb6fe1c4; related links: http://www.alz.org/facts/ (+Video) (2015 Alzheimer's Disease Facts and Figures. Learn. Share. Act.) and http://brain.oxfordjournals.org/content/early/2016/01/07/brain.awv379  (Pharmacological targeting of CSF1R inhibits microglial proliferation and prevents the progression of Alzheimer’s-like pathology. Adrian Olmos-Alonso, Sjoerd T. T. Schetters, Sarmi Sri, Katharine Askew, Renzo Mancuso, Mariana Vargas-Caballero, Christian Holscher, V. Hugh Perry, and Diego Gomez-Nicola. Published in Brain. A Journal of Neurology. DOI: http://dx.doi.org/10.1093/brain/awv379 awv379 First published online: 8 January 2016. [Summary: The proliferation and activation of microglial cells is a hallmark of several neurodegenerative conditions. This mechanism is regulated by the activation of the colony-stimulating factor 1 receptor (CSF1R), thus providing a target that may prevent the progression of conditions such as Alzheimer’s disease. However, the study of microglial proliferation in Alzheimer’s disease and validation of the efficacy of CSF1R-inhibiting strategies have not yet been reported. In this study we found increased proliferation of microglial cells in human Alzheimer’s disease, in line with an increased upregulation of the CSF1R-dependent pro-mitogenic cascade, correlating with disease severity. Using a transgenic model of Alzheimer’s-like pathology (APPswe, PSEN1dE9; APP/PS1 mice) we define a CSF1R-dependent progressive increase in microglial proliferation, in the proximity of amyloid-β plaques. Prolonged inhibition of CSF1R in APP/PS1 mice by an orally available tyrosine kinase inhibitor (GW2580) resulted in the blockade of microglial proliferation and the shifting of the microglial inflammatory profile to an anti-inflammatory phenotype. Pharmacological targeting of CSF1R in APP/PS1 mice resulted in an improved performance in memory and behavioural tasks and a prevention of synaptic degeneration, although these changes were not correlated with a change in the number of amyloid-β plaques. Our results provide the first proof of the efficacy of CSF1R inhibition in models of Alzheimer’s disease, and validate the application of a therapeutic strategy aimed at modifying CSF1R activation as a promising approach to tackle microglial activation and the progression of Alzheimer’s disease.])>