Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice

摘要

Abnormal accumulation of β-amyloid (Aβ) in Alzheimer's disease (AD) is associated with prominent brain inflammation. Whereas earlier studies concluded that this inflammation is detrimental, more recent animal data suggest that at least some inflammatory processes may be beneficial and promote Aβ clearance. Consistent with these observations, overproduction of transforming growth factor (TGF)-β 1 resulted in a vigorous microglial activation that was accompanied by at least a 50/100 reduction in Aβ accumulation in human amyloid precursor protein (hAPP) transgenic mice.