Topic: Aβ plaques

In previous studies, we identified low-perfused vascular abnormalities, termed “vascular scars”, surrounding A-beta plaques in Alzheimer's disease mouse models. We hypothesized that these vascular scars result from non-productive angiogenesis, a process in which total or partial reduction of the DLL4/NOTCH pathway leads to erratic angiogenesis and disassembly of vessels into non-conducting structures1. In this study, our objective was to investigate whether restoring the NOTCH pathway in brain endothelial cells could enhance vessel stability around A-beta plaques. To this aim, we injected the

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. Accumulating experimental evidence shows the important role of tumor necrosis factor-α (TNF-α) signaling in AD, but the exact role of TNF-α in AD is still not completely understood. Although TNF-inhibitors are successfully used for treatment of several autoimmune diseases, like rheumatoid arthritis, total inhibition of TNF-α can cause adverse side effects in neurological diseases. This is attributed to the opposing roles of the two receptors of TNF-α. TNF receptor 1 (TNFR1) predominantly

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder associated with memory and cognitive deficits. Both amyloid β (Aβ) deposition and inflammatory response occur in the early course of AD, but the progression of cognitive impairment and its relationship with Aβ and neuroinflammation have not been fully understood. Dieckol is a phenolic compound from brown algae and has been reported to possess several health benefits. In particular, our previous studies have shown that the compound exerts the neuroprotective effects by inhibiting amyloidogenesis, oxidative stress and inflamma

Alterations along the brain-gut axis participate in the pathogenesis of neurodegenerative diseases. Recent data suggest that the gut microbiota partially exerts its action by modulating neuroinflammation. Interestingly, neuroinflammation has been postulated as one of the leading causes of Alzheimer’s Disease (AD). Therefore, targeting brain inflammation has been suggested as a promising therapeutic strategy to cope with AD. In this regard, neuroinflammation has been related to the soluble epoxide hydrolase (sEH) enzyme, which is upregulated in the brains of AD patients and mice models of AD. C