Background: Glycolysis in astrocytes may govern amyloid accumulation and cytotoxicity. Results: Inhibiting astrocytic PFKFB3 results in an accumulation of amyloid protein and vulnerability to A␤ cytotoxicity. In APP transgenic mice, reactive astrogliosis parallels the increased A␤ burden and PFKFB3 activity in an age-dependent manner. Conclusion: Astrocytic glycolysis is a key component for amyloid toxicity. Significance: The bioenergetic mechanism in astrocytes may contribute to AD pathology.

Our findings suggest that predisposition to autoimmunity, and immune/inflammatory activation, may be associated with autistic regression.

Overexpressed secretory phospholipase A2 (sPLA2) is found in many inflammatory diseases and various types of cancer. sPLA2 can catalyze the hydrolysis of phospholipid sn-2 ester bond to lysophosphatidylcholine and free...

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