Modification of amyloid-beta peptide aggregation via photoactivation of strained Ru(ii) polypyridyl complexes

Abstract

Photoactivation of a series of Ru(ii) polypyridyl complexes leads to ligand exchange and modulation of amyloid-beta peptide aggregation of relevance to Alzheimer's disease.

Benzothiazolium Derivative-Capped Silica Nanocomposites for β-Amyloid Imaging In Vivo

“… 34 Besides, the 2MXU structure has a well-defined hydrophobic cleft and 12 β-strand filaments providing sufficient surface area for modeling the interactions with the probes. 35 Therefore, the β-amyloid (Aβ 1–42 ) aggregate protein model (PDB ID: 2MXU) was chosen to evaluate the interaction between Aβ 1–42 aggregates and SZIs. The results were processed using Autodock Tools 1.5.6, PyMOL, and Python software, which are shown in the licorice form and molecular surface form.…”

The Development of Ru(II)-Based Photoactivated Chemotherapy Agents

“…It was worth mentioning that the photo-cytotoxicity increased by 2 orders of magnitude for 28 and 29 . According to the same idea, a series of Ru(II) complexes with steric bulk have been studied in depth [ 64 , 65 , 66 , 67 , 68 ].…”

Simultaneous binding of heme and Cu with amyloid β peptides: active site and reactivities

“…[1][2][3][4][5][6] The two main histopathological features of AD are the formation of extracellular deposits of fibrillar peptides called senile plaques and the generation of intraneuronal fibrillar tangles. [6][7][8] The main constituent of the extracellular deposits is the amyloid β (Aβ) peptide, which is ∼40-42 amino acid residues long and is generated from a transmembrane protein called amyloid precursor protein (APP) by the action of secretase enzymes. 6,8,9 On the other hand, the intraneuronal fibrillar tangles are made of twisted strands of hyperphosphorylated tau protein.…”

“…[6][7][8] The main constituent of the extracellular deposits is the amyloid β (Aβ) peptide, which is ∼40-42 amino acid residues long and is generated from a transmembrane protein called amyloid precursor protein (APP) by the action of secretase enzymes. 6,8,9 On the other hand, the intraneuronal fibrillar tangles are made of twisted strands of hyperphosphorylated tau protein. 10,11 The amyloid imbalance in the AD brain and extracellular deposition of Aβ plaques fall under the "amyloid cascade hypothesis" whereas the formation of intraneuronal fibrillar tangles consisting of hyperphosphorylated tau protein is under tauopathy.…”