The Nun study: Clinically Silent Alzheimer’s disease

One of the main ways that you can determine if a person had Alzheimer’s disease is by analyzing their brain tissue after they pass way. In patients with Alzheimer’s disease, one of the main determinants includes the presence of Beta amyloid plaques and Neurofibrillary tangles. As mentioned in the previous week, Beta amyloid plaques occur through the improper mechanism and accumulation of the protein tau.

This study mainly examined the brain tissues particularly the CA-1 portion of the hippocampus of patients for Alzheimer’s disease (AD) lesions. These AD lesions included beta amyloid plaques and tangles. The Nun study was very similar to the BLSA study with the only exception that this study mainly focused on the female population. The main basis to this study was the presence of AD lesions in elderly individuals with no symptoms of Alzheimer’s. The BLSA study helped to provide evidence that was a significant amount of AD lesions in patients that were primarily men. The Nun study helped to complement the BLSA study with the only exception of the gender of the population. The criteria used for the Nun study were very similar to that of the BLSA study and included mainly subjects that were age controls, asymptomatic Alzheimer’s disease (ASYMAD), Mild Cognitive Impairment (MCI) and Alzheimer’s disease (AD).

Diagnostic tests such as CERAD and Braak staging was used to determine the severity of both the neurofibrillary tangles and B-amyloid plaques. APOE genotyping was also conducted for the polymorphisms of APOE as it is one of the possible risk factors for Alzheimer’s disease. There are various isoforms of APOE gene: E2, E3 AND E4 variants. According to research, a high frequency in E4 variant is considered as one of the risk factors for Alzheimer’s disease.

Based on the results obtained, it was confirmed that in patients with the increase in hypertrophied neuronal cells in the hippocampus, there was a protective effect that led them to be asymptomatic. This was indicated as possibly one of its compensatory mechanisms. The hypertrophy in neuronal cell bodies, nucleus and nucleolus was determined as one of its ability to adapt with the constant damage within the brain tissue. It was also confirmed that in patients with high frequency of E2 alleles, there were no symptoms of Alzheimer’s Disease even with moderate to high levels of AD lesions. One of most interesting aspect of this article was the association between high levels of E2 allele frequency and the increased amount of hypertrophied neuronal cells that acts as a compensatory mechanism that helps in preventing the symptoms of Alzheimer’s Disease. I enjoyed the thorough diagrams that were found within the article and the content of this research. However, I hope this article is a stepping stone to further research that will help support the association between E2 allele frequency and ASYMAD.