Alzheimer's disease is a rising threat for modern societies as more and more people reach old age. To date, there is no effective treatment for this condition. In this study, we investigated the potential of Glycyrrhiza uralensis to counteract amyloid-β toxicity, one of the key features of Alzheimer's disease. An LC-MS/MS analysis revealed glycyrrhizic acid and glycosylated forms of isoliquirit...

A multimodal, β-amyloid-targeted contrast agent was synthesized and studied in vitro. The agent has a higher relaxivity than a clinically approved contrast agent and interacts with β-amyloid aggregates producing changes in relaxation rate and fluorescence emission.

Inflammatory processes are important in the pathogenesis of Alzheimer's disease and in response to amyloid-β immunotherapy. We investigated the expression of multiple inflammatory markers in the brains of 28 non-immunized patients with Alzheimer's disease and 11 patients with Alzheimer's disease immunized against amyloid-β42 (AN1792): microglial ionized calcium-binding adaptor Iba-1, lysosome m...

In vivo imaging of fibrillar β-amyloid deposits may assist clinical diagnosis of Alzheimer's disease (AD), aid treatment selection for patients, assist clinical trials of therapeutic drugs through subject selection, and be used as an outcome measure. A recent phase III trial of [18F]flutemetamol positron emission tomography (PET) imaging in 106 end-of-life subjects demonstrated the ability to i...

The pathological hallmark of Alzheimer's disease is brain deposition of senile plaques composed predominantly of amyloid fibrils. These conformational structures, characteristic of many other human disorders, are formed mainly by the amyloid-β peptide Aβ42. This peptide, which is primarily disordered and soluble as an isolated monomer, can undergo an aggregation and fibrillation process that re...

early brain dysfunction that could be assessed as an outcome measure in response to therapeutic interventions. very mildly impaired humans who are developing AD pathology, the sleep-wake cycle may be a useful indicator of accumulation. If analogous abnormalities in the sleep-wake cycle are present in cognitively normal and β caused by A fluctuation and normal sleep patterns. These findings sugg...

Peptide/protein hormones could be stored as non-toxic amyloid-like structures in pituitary secretory granules. ACTH and β-endorphin are two of the important peptide hormones that get co-stored in the pituitary secretory granules. Here, we study molecular interactions between ACTH and β-endorphin and their colocalization in the form of amyloid aggregates. Although ACTH is known to be a part of A...

In Alzheimer's disease, soluble amyloid-β causes synaptic dysfunction and neuronal loss. Receptors involved in clearance of soluble amyloid-β are not known. Here we use short hairpin RNA screening and identify the scavenger receptor Scara1 as a receptor for soluble amyloid-β expressed on myeloid cells. To determine the role of Scara1 in clearance of soluble amyloid-β in vivo, we cross Scara1 nu...

Experimental studies have reported that the amyloid-β proteins can form pores in cell membranes, and this could be one possible source of toxicity Alzheimer's disease. Dissociation these therefore a potential therapeutic approach. It is known high photon density free-electron laser experiments laser-induced nonequilibrium molecular dynamics simulations (NEMD) dissociate amyloid fibrils at speci...

β-amyloid peptides (Aβ) are generated in intracellular compartments of neurons and secreted to form cytotoxic fibrils plaques. Dysfunctional membrane trafficking contributes aberrant Aβ production Alzheimer's disease. Endosomes represent one the major sites for recently Golgi has re-emerged also as a location amyloid precursor protein (APP) processing production. Based on recent findings, here ...