Topic: brain-gut axis

Alzheimer’s disease (AD) is an age-related neurodegenerative disease characterized by cerebral accumulation of extracellular plaques of aggregated amyloid-β (Aβ) peptide, neurofibrillary tangles composed of truncated and hyperphosphorylated Tau protein, both leading to synaptic loss, and neuronal death. To ensure cerebral homeostasis, several elimination mechanisms exist for these toxic proteins. Recently, a complex mechanism based on exchanges between different extracellular space has been identified in the brain: the glymphatic system. Our aim is to study how the brain-gut axis participates

Alzheimer's disease (AD) presents a complex challenge, increasingly linked to the gut microbiota’s role in its development. This study examines changes in the gut microbiome of AD patients, focusing on the reduction of certain bacteroides strains and their metabolite, MEDICA, known for anti-inflammatory effects. However, its direct influence on AD pathology is unclear. We suggest that MEDICA supplementation might improve cognitive function by interacting with the brain-gut axis. To explore this, we assessed the impact of MEDICA on amyloid plaque formation and neuroinflammation. Our results ind

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