The Future of Alzheimer

Alzheimer is a type of neurodegenerative disease that causes problems with memory, thinking, and behavior.  The symptoms of this neurodegenerative disease develop slowly, and get worse over time, causing interference with daily tasks, and eventually death.  One of the main mechanism that causes this disease is the accumulation of misfolded beta amyloid peptide, which causes a change in both the central and peripheral nervous system.  The accumulation of misfolded beta amyloid peptide causes an innate response of the brain, which activates microglia, and astrocytes. It also releases immune inflammatory molecules like cytokines, and acute phase protein.  The activation of these immune molecules has both advantages and disadvantages. For instance, activation of the microglia cells causes phagocytosis of the misfolded protein, however, it also causes release of neurotoxic that causes neuronal injury.  

In Dr. Spani’s study, she looked at the role of congenital deficiency on beta amyloid protein pathology, in vivo, and from crossbreeding PSAPP (mice with alzheimer) and Rag2 ko mice (mice lacking B and T cell), generated B cell and T cell ablation.  Then, in the second part of her experiment, the effects of adaptive immunity of the PSAPP mice reconstructed with Rag2 ko mice bone marrow was examined. For both parts of her experiment, she found that the immune cells yielded cerebral beta amyloid aggregation, in addition to greater beta amyloid protein clearance, which she concluded was from the microglial cells.  This result essentially shows how the ablation of functional B and T cells led to increased clearance of beta amyloid protein by microglial cells, and reduced levels of misfolded beta amyloid proteins in the brain. Thus, the findings of this study could potentially be future therapeutics to Alzheimer. However, people do need to consider that even though this mechanism does control toxic neuroinflammatory response of beta amyloid protein aggregation, it also increases amyloid plaque deposition.  

The article “Beta-amyloid dimers found in brains of patients with Alzheimer's,” focused on the chemical makeup of the beta amyloid protein.  This study was different from Dr. Spani’s study because by looking at the brain tissue of normal patients, Dr. Vasquez found out beta amyloid protein form dimers that are linked together by covalent bonds, which are extremely hard to break during brain extraction.  Since these researchers can’t work with brains of living patients with Alzheimer’s because of certain ethical issues, they are looking forward to determine if these beta amyloid dimers are present in the CSF of patients with Alzheimer. After examining the CSF of patients with ALzheimer’s, these researchers are planning to start clinical trials to relate the presence of these dimers to the stages of Alzheimer.  On the other hand, this study was similar to Dr. Spani’s study since this study also found high accumulation of beta amyloid proteins in the cerebral brain tissue of Alzheimer patients. Therefore, if we look at the beta amyloid protein dimers, and ablate functional B and T cells, this can save the lives of many patients affected with Alzheimer.

Works Cited

Institute for Research in Biomedicine (IRB Barcelona). (2018, April 17). Beta-amyloid dimers found in brains of patients with Alzheimer's. ScienceDaily. Retrieved December 10, 2018 from www.sciencedaily.com/releases/2018/04/180417115709.htm

Späni, C. et al. (2015). Reduced β-amyloid pathology in an APP transgenic mouse model of Alzheimer’s disease lacking functional B and T cells. Acta Neuropathologica Communications, 3(71), https://doi.org/10.1186/s40478-015-0251-x.