We performed an enzymatic screening of synthetic peptides based on β-amyloid precursor protein substrates. The template peptide sequence was a decapeptide derived from our previous study, which determined several effective unnatural amino acids. In this new libraries containing some acid compounds were prepared in the solid phase and digested with β-site amyloid protein-cleaving enzyme. reactio...

Abstract A key hallmark of Alzheimer’s disease is the extracellular deposition amyloid plaques composed primarily amyloidogenic amyloid-β (Aβ) peptide. The Aβ peptide a product sequential cleavage Amyloid Precursor Protein, first step which gives rise to C-terminal Fragment (C99). Cleavage C99 by γ-secretase activity releases several lengths and Aβ42 isoform in particular has been identified as...

BACKGROUND Polybasic helical peptides, such as peptide p5, bind human amyloid extracts and synthetic amyloid fibrils. When radiolabeled, peptide p5 has been shown to specifically bind amyloid in vivo thereby allowing imaging of the disease. Structural requirements for heparin and amyloid binding have been studied using analogs of p5 that modify helicity and chirality. METHODS Peptide-ligand i...

INTRODUCTION In Alzheimer's disease, accumulation and pathological aggregation of amyloid β-peptide is accompanied by the induction of complex immune responses, which have been attributed both beneficial and detrimental properties. Such responses implicate various cell types of the innate and adaptive arm of the immunesystem, both inside the central nervous system, and in the periphery. To inve...

Amyloid-β peptides interact with cell membranes in the human brain and are associated with neurodegenerative diseases, such as Alzheimer's disease. An emerging explanation of the molecular mechanism, which results in neurodegeneration, places the cause of neurotoxicity of the amyloid- peptides on their potentially negative interaction with neuronal membranes. It is known that amyloid-β peptides...

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that affects regions of the brain that control cognition, memory, language, speech and awareness to one’s physical surroundings. The pathological initiation and progression of AD is highly complex and its prevalence is on the rise. In his study, Alzheimer's disease was induced with single injection of amyloid-β (Aβ) peptides (...

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...

The progression of Alzheimer's disease is causatively linked to the accumulation of amyloid-β aggregates in the brain, however, it is not clear how the amyloid aggregates initiate the death of neuronal cells. The in vitro toxic effects of amyloid peptides are most commonly examined using the human neuroblastoma derived SH-SY5Y cell line and here we show that differentiated neuron-like SH-SY5Y c...

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that affects regions of the brain that control cognition, memory, language, speech and awareness to one’s physical surroundings. The pathological initiation and progression of AD is highly complex and its prevalence is on the rise. In his study, Alzheimer's disease was induced with single injection of amyloid-β (Aβ) peptides (...