The amyloid beta (Aβ) fibrillar aggregate is the hallmark of Alzheimer's disease (AD).
Disassembling preformed fibril or inhibiting Aβ aggregation is considered as a therapeutic …

Fibrillary aggregates of amyloid-β (Aβ) are the pathological hallmark of Alzheimer's disease
(AD). Clearing Aβ deposition or inhibiting Aβ aggregation is a promising approach to treat …

Amyloid beta (Aβ) peptide aggregates rapidly into the soluble oligomers, protofibrils and
fibrils to form senile plaques, a neurotoxic component and pathological hallmark of …

Alzheimer's disease (AD) is an irreversible, progressive neurodegenerative disorder that
may account for approximately 60-70% of cases of dementia worldwide. AD is characterized …

Alzheimer's disease (AD) is associated with the aberrant self-assembly of amyloid-β (Aβ)
protein into fibrillar deposits. The disaggregation of Aβ fibril is believed as one of the major …

The accurate prediction of protein–ligand binding free energies with tractable computational
methods has the potential to revolutionize drug discovery. Modeling the protein–ligand …

According to clinical studies, the development of Alzheimer's disease (AD) is linked to the
abnormal aggregation of amyloid-β (Aβ) peptides into toxic soluble oligomers, protofibrils as …

4-Sulfanyl-substituted 1, 2, 3-triazoles were provided regioselectively with good yields and
broad scope via consecutive t-BuOK-promoted dephosphinylation of 1-phosphinyl-2 …

The clinical signature of Alzheimer's disease (AD) is the deposition of aggregated Aβ fibrils
that are neurotoxic to the brain. It is the major form of dementia affecting older people …

Alzheimer′ s disease (AD) is related to the misfolding and aggregation of amyloid-β (Aβ)
protein, and its major pathological hallmark is fibrillary β-amyloid plaques. Impeding the …