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Learn MoreALSP is a CSF1R-deficiency dementia associated with increased CSF2 expression; Monoallelic deletion of Csf2 rescues most behavioral deficits and histopathological changes in Csf1r+/- mice by preventing microgliosis and eliminating most microglial transcriptomic alterations, including those indicative of oxidative stress and demyelination; Elevation of Csf2 transcripts and of several CSF-2 downstream targets in the brains of ALSP patients demonstrates that the mechanisms identified in the mouse model are functional in man.; Our data provide new insights into the mechanisms underlying ALSP and identify CSF-2 as a therapeutic target. SOURCE: Deyou Zheng (deyou.zheng@einstein.yu.edu) - Albert Einstein College of Medicine
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