Amyloid-β plaques and neurofibrillary tangles are the main neuropathological hallmarks in Alzheimer’s disease (AD), the most common cause of dementia in the elderly. However, it has become increasingly apparent that neuroinflammation plays a significant role in the pathophysiology of AD. This review summarizes the current status of neuroinflammation research related to AD, focusing on the connections between neuroinflammation and some inflammation factors in AD. Among these connections, we discuss the dysfunctional blood–brain barrier and alterations in the functional responses of microglia and astrocytes in this process. In addition, we summarize and discuss the role of intracellular signaling pathways involved in inflammatory responses in astrocytes and microglia, including the mitogen-activated protein kinase pathways, nuclear factor-kappa B cascade, and peroxisome proliferator–activated receptor-gamma transcription factors. Finally, the dysregulation of the control and release of pro- and anti-inflammatory cytokines and classic AD pathology (amyloid plaques and neurofibrillary tangles) in AD is also reviewed.

Stroke is the second leading cause of death among adults worldwide. (-)-Epigallocatechin-3-gallate (EGCG) has been demonstrated to exhibit neuroprotective functions in cerebral ischemia/reperfusion injury. However, the underlying mechanisms in this process and its contribution to the protection function remain unknown. The current study examined the neuroprotective effects of EGCG after transient middle cerebral artery occlusion (tMCAO) in rats. tMCAO for 120 min was induced in male Sprague-Dawley rats treated with EGCG (50 mg/kg, i.p.) or Vehicle immediately after reperfusion. Neurological score, infarct ratio and inflammation-related molecules (assessed by 2,3,5-triphenyltetrazolium chloride, enzyme-linked immunosorbent assays, quantitative real-time PCR or western blotting) were estimated at 24 h after operation. EGCG prevented the impairment of neurological function and decreased the infarct volume, compared with the Vehicle group. The inflammation-related molecules TNF-α, IL-1β, IL-6 levels usually caused by ischemia/reperfusion were significantly ameliorated by EGCG. EGCG also inhibited the upregulation of nuclear factor-kappa B/p65 (NF-κB/p65), and induction of cyclooxygenase 2 and inducible nitric oxide synthase. The present study indicates that EGCG may be a promising therapeutic agent for cerebral ischemia/reperfusion injury through attenuation of inflammation.