We introduce a mathematical model of the in vivo progression of Alzheimer's disease with focus on the role of prions in memory impairment. Our model consists of differential equations that describe the dynamic formation of β-amyloid plaques based on the concentrations of Aβ oligomers, PrP(C) proteins, and the Aβ-x-Aβ-PrP(C)complex, which are hypothesized to be responsible for synaptic toxicity....

Alzheimer's disease (AD) is widely considered to be caused by amyloid-β peptide (Aβ) accumulation in the brain. Aβ is excised from amyloid-β precursor protein through sequential cleavage by β-secretase 1 (BACE1) and γ-secretase. Thus, BACE1 inhibition could prevent Aβ accumulation. Here, we identified myo-inositol hexakisphosphate (IP6) as a BACE1 inhibitory molecule in rice grain extract and d...

The propensity of amyloid-β (Aβ) peptide to self-assemble into highly ordered amyloid structures lies at the core of their accumulation in the brain during Alzheimer's disease. By using all-atom explicit solvent replica exchange molecular dynamics simulations, we elucidated at the atomic level the intrinsic determinants of the pH-dependent dimerization of the central hydrophobic segment Aβ(12-2...

Introduction: Alzheimer disease (AD) is a neurodegenerative disorder characterized by the progressive loss of memory and other cognitive functions. Protein kinase Cε (PKCε) is an isoform that most effectively suppresses amyloid beta (Aβ) production and synaptic loss. Methods: In this study, spatial learning and memory for treated rats were evaluated by the Morris water maze test. The activity ...

Alzheimer's disease (AD) is a neurodegenerative pathology commonly characterized by a progressive and irreversible deterioration of cognitive functions, especially memory. Although the etiology of AD remains unknown, a consensus has emerged on the amyloid hypothesis, which posits that increased production of soluble amyloid β (Aβ) peptide induces neuronal network dysfunctions and cognitive defi...

The formation of amyloid β (Aβ) fibrils is crucial in initiating the cascade of pathological events that culminates in Alzheimer's disease. In this study, we investigated the mechanism of Aβ fibril formation from hydrodynamically well defined species under controlled aggregation conditions. We present a detailed mechanistic model that furnishes a novel insight into the process of Aβ42 fibril fo...

Objective: Alzheimer's disease is a neurodegenerative disorder characterized by accumulation of amyloid beta in the hippocampus. In recent decades, herbal medicine has been widely used to treat many neurodegenerative disorders,as in comparison to conventional drugs, herbal remedies exert minimal side effects. Here, the effects of thymoquinone, as the main active component of Nigella sativa, on ...

Background Among other emerging amyloid-targeting blood-based biomarkers, Multimer Detection System-Oligomeric Amyloid-β (MDS-OAβ) measures dynamic changes in concentration of oligomeric amyloid-β (OAβ), which is considered the main pathogenic culprit Alzheimer’s disease (AD), plasma after spiking with synthetic (Aβ). We aimed to investigate predictability MDS-OAβ on amyloid Positron Emission T...

Increased APP (amyloid precursor protein) processing causes β-amyloid (Aβ) accumulation in autosomal dominant Alzheimer's disease (AD), but it is unclear if it also affects sporadic Aβ accumulation. We tested healthy controls and patients with mild cognitive symptoms (N=331) in the BioFINDER study, using cerebrospinal fluid (CSF) Aβ40 as a surrogate for amyloidogenic APP processing. We find tha...

A glycopolymer carrying trehalose was found to suppress the formation of amyloid fibrils from the amyloid β peptide (1-42) (Aβ), as evaluated by thioflavin T assay and atomic force microscopy. Glycopolymers carrying sugar alcohols also changed the aggregation properties of Aβ, and the inhibitory effect depended on the type of sugar and alkyl side chain. Neutralization activity was confirmed by ...