Alzheimer's Disease: A Symptomatic Analysis

As medicine continues to progress, treatment options for once incurable diseases are becoming increasingly more prevalent and effective. Unfortunately, treatment options for those suffering from Alzheimer’s disease have not experienced similar progress. Current Alzheimer’s treatment remains symptomatic, addressing solely the cognitive deficits associated with Alzheimer’s while failing to halt the progression of the disease and its neurodegenerative effects. In an attempt to further diverse treatment options for patients currently suffering from Alzheimer’s, novel protein receptors in the brain are being examined. Additionally, by identifying the structural motifs that define the pharmacophores of molecules which appear to aid in Alzheimer’s
Essentially, acetylcholinesterase inhibitors function by preventing the degradation of acetylcholine, one of the primary neurotransmitters responsible for, among a myriad of other things, learning and memory functions within the brain. While acetylcholinesterase inhibitors are effective in terms of increasing the concentration of acetylcholine in the brain, they do not address one of the most important aspects of Alzheimer’s disease, its pathogenesis, or progression in the brain. Although not completely understood with regards to function, the 5-HT6 receptor, also known as the 5-hydroxytrpytamine receptor, binds to serotine, otherwise known as 5-hydroxytryptamine. As a neurotransmitter, serotonin exerts its control over numerous functions within the brain, chief among those being learning and memory. In addition, due to the nature of the 5-HT6 receptor being located on the surface of cells, treatment options that target the receptor can potentially induce improved memory and cognitive function through multiple signaling pathways. Overall, this would lend itself to potentially more sustained cognitive improvements relative to current treatment, as
The process of chelating is most commonly described as the binding of metal ions to organic molecules. As it has been addressed in the past literature, treatments of Alzheimer’s disease is primarily symptomatic. At the present state, treatment is designed to alleviate symptoms without halting disease progression. Amyloid beta peptide polymerization is considered to be one of the hallmarks of Alzheimer’s progression within the brain. Therefore, by developing treatment strategies to inhibit the aggregation of amyloid beta peptides, there is potential to inhibit the progression of Alzheimer’s disease beyond traditional approaches, such as acetylcholine replacement therapy. One means of inhibiting beta amyloid plaque formation is through the sequestering of copper ions; since copper ion concentration is elevated within plaques. Cooper ions have been shown to induce the formation of these extra-neuronal plaques. In addition, copper ions within beta amyloid plaques have been linked to the production of reactive oxygen species. Ultimately, this oxidative stress leads to increased neurotoxicity, and finally cell apoptosis. Interestingly, the compounds in the current study designed to chelate with copper ions have been