It has been hypothesized that alterations in the composition of the gut microbiota might be associated with the onset of certain human pathologies, such as Alzheimer disease, a neurodegenerative syndrome associated with cerebral accumulation of amyloid-β fibrils. It has been shown that bacteria populating the gut microbiota can release significant amounts of amyloids and lipopolysaccharides, which might play a role in the modulation of signaling pathways and the production of proinflammatory cytokines related to the pathogenesis of Alzheimer disease. Additionally, nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-β. This suggests that modulating the gut microbiome and amyloidogenesis through specific nutritional interventions might prove to be an effective strategy to prevent or reduce the risk of Alzheimer disease. This review examines the possible role of the gut in the dissemination of amyloids, the role of the gut microbiota in the regulation of the gut–brain axis, the potential amyloidogenic properties of gut bacteria, and the possible impact of nutrients on modulation of microbiota composition and amyloid formation in relation to the pathogenesis of Alzheimer disease.

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Role of gut microbiota and nutrients in amyloid formation and pathogenesis of Alzheimer disease

Recent advancements in liposomes targeting strategies to cross blood-brain barrier (BBB) for the treatment of Alzheimer's disease.

Physiological roles of the intermediate conductance, Ca2+-activated potassium channel Kcnn4. Vol. 279 (2004) 47681–47687

Amyloid-beta (Aβ) accumulation in the brain is believed to play a central role in Alzheimer’s disease (AD) pathogenesis, and the common late-onset form of AD is characterized by an overall impairment in Aβ clearance. Therefore, development of nanomedicine that can facilitate Aβ clearance represents a promising strategy for AD intervention. However, previous work of this kind was concentrated at the molecular level, and the disease-modifying effectiveness of such nanomedicine has not been investigated in clinically relevant biological systems. Here, we hypothesized that a biologically inspired nanostructure, apolipoprotein E3–reconstituted high density lipoprotein (ApoE3–rHDL), which presents high binding affinity to Aβ, might serve as a novel nanomedicine for disease modification in AD by accelerating Aβ clearance. Surface plasmon resonance, transmission electron microscopy, and co-immunoprecipitation analysis showed that ApoE3–rHDL demonstrated high binding affinity to both Aβ monomer and oligomer. It al...

Lipoprotein-Based Nanoparticles Rescue the Memory Loss of Mice with Alzheimer’s Disease by Accelerating the Clearance of Amyloid-Beta

α-Mangostin from Garcinia mangostana Linn: An updated review of its pharmacological properties

Α-mangostin, a polyphenolic xanthone derivative from mangosteen, attenuates β-amyloid oligomers-induced neurotoxicity by inhibiting amyloid aggregation.

KCa31 has been suggested to be involved in regulating cell activation, proliferation, and migration in multiple cell types, including airway inflammatory and structural cells However, the contributions of KCa31 to airway inflammation and remodeling and subsequent airway hyperresponsiveness (AHR) in allergic asthma remain to be explored The main purpose of this study was to elucidate the roles of KCa31 and the potential therapeutic value of KCa31 blockers in chronic allergic asthma Using real-time PCR, Western blotting, or immunohistochemical analyses, we explored the precise role of KCa31 in the bronchi of allergic mice and asthmatic human bronchial smooth muscle cells (BSMCs) We found that KCa31 mRNA and protein expression were elevated in the bronchi of allergic mice, and double labeling revealed that up-regulation occurred primarily in airway smooth muscle cells Triarylmethane (TRAM)–34, a KCa31 blocker, dose-dependently inhibited the generation and maintenance of the ovalbumin-induced airw

Hong-Zhuan Chen

Papers

Α-mangostin, a polyphenolic xanthone derivative from mangosteen, attenuates β-amyloid oligomers-induced neurotoxicity by inhibiting amyloid aggregation.

Targeted inhibition of KCa3.1 channel attenuates airway inflammation and remodeling in allergic asthma