A Comparative Interaction between Copper Ions with Alzheimer's β Amyloid Peptide and Human Serum Albumin

The interaction of Cu2+ with the first 16 residues of the Alzheimer's amyliod β peptide, Aβ(1–16), and human serum albumin (HSA) were studied in vitro by isothermal titration calorimetry at pH 7.2 and 310？K in aqueous solution. The solvation parameters recovered from the extended solvation model indicate that HSA is involved in the transport of copper ion. Complexes between Aβ(1–16) and copper ions have been proposed to be an aberrant interaction in the development of Alzheimer's disease, where Cu2+ is involved in Aβ(1–16) aggregation. The indexes of stability indicate that HSA removed Cu2+ from Aβ(1–16), rapidly, decreased Cu-induced aggregation of Aβ(1–16), and reduced the toxicity of Aβ(1–16) + Cu2+ significantly. 1. Introduction One of the hallmarks of Alzheimer's disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Beta amyloid is a protein fragment snipped from an amyloid precursor protein (APP). In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques. Alzheimer's disease and heart disease were made worse by excess copper and iron. Researchers are still trying to fully understand how its plaques and tangles lead to memory loss and other symptoms and how to reverse those changes to prevent or stop the disease. However, there are treatments available today that can help patients manage the symptoms of Alzheimer's disease and delay its progression. Acetylcholine helps pass messages between certain brain cells involved in memory. In Alzheimer's disease, these brain cells start to die and the amount of acetylcholine is reduced. Cholinesterase inhibitors reduce the breakdown of acetylcholine and increase its levels in the brain. This reduces some of the symptoms of Alzheimer's disease. HSA carries metal ions, including physiological Ca2+, Zn2+, Co2+, and Cu2+, as well as toxic Cd2+ and Ni2+ [1–5]. Although the etiology of cognitive impairment in Alzheimer's disease (AD) is not fully understood, it has been reported that acetylcholine-producing neurons degenerate in the brains of patients with Alzheimer's disease. The degree of this cholinergic loss has been correlated with degree of cognitive impairment and density of amyloid plaque. Galantamine, a tertiary alkaloid, is a competitive and reversible inhibitor of acetylcholinesterase. It is possible to postulate galantamine's action therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine through