Purpose: Monoclonal gammopathy of undetermined significance (MGUS) is a plasma cell dyscrasia. It is known that MGUS has an increased risk of progression to multiple myeloma (MM), and also prepares the ground for diseases such as Waldenstrom macroglobulinemia (WM), non-Hodgkin lymphoma, and chronic lymphocytic leukemia (CLL). Our study aimed to evaluate whether some important p53 pathway genes differ in terms of expression in MGUS and healthy individuals. Materials and methods: For the study, bone marrow was collected from 8 healthy individuals and 8 individuals diagnosed with MGUS, and RNA samples were isolated. Expression levels of various genes involved in the p53 pathway were compared using the RT2-profiler PCR array. β-actin housekeeping gene expression level was used for normalization. The Pearson Correlation analysis and Receiver Operating Characteristic (ROC) analysis were conducted. Results: Among the genes whose expression levels were examined in this study, it was determined that the expression level of only the GADD45A gene decreased significantly in MGUS compared to the control group (p=0.027). Pearson correlation data showed that GADD45A gene expression was highly correlated with 12 of the other genes (APAF1, CDK4, PCNA, BAX, CDKN2A, CASP9, CHECK2, MDM2, RB1, P53, BCL2, CHEK1) examined in the p53 pathway (r>0.7). In addition, according to the ROC analysis, GADD45A is detected to have a strong discrimination power between MGUS and healthy individuals (AUC=0.797 and p=0.015). Conclusion: The decreased expression of the GADD45A gene in the MGUS group compared to the control group may be useful as a new biomarker to detect the risk of progression from MGUS to MM.
Dementia is mostly caused by neurodegenerative diseases like Alzheimer’s disease (AD). AD is the most common form of dementia. It is caused by both genetic and environmental factors. Due to neuronal death in a number of brain regions, including the hippocampus, entorhinal areas, temporal lobe, and cingulate cortex, AD causes memory loss and gradual cognitive impairment. The condition’s two main pathogenic components are intracellular neurofibrillary tangles created by clusters of hyperphosphorylated tau protein and amyloid plaques made up of extracellular amyloid (Aβ) peptide aggregates. In contrast to the APOE- ε4 allele, which was found to have a significant impact on late-onset AD, presenilin 1, presenilin 2, amyloid precursor protein were genetic risk factors that were causal for early-onset AD. Misfolded proteins accumulate within the neuron, causing prolonged cellular stress in AD, a progressive neurodegenerative disease. Neurofibrillary tangles and senile plaques are two of the neuropathological hallmarks of Alzheimer’s disease that lead to the destruction of synapses and the death of neurons. AD is mostly caused by the death of nerves, particularly cholinergic nerves. In the absence of these cholinergic neurons, acetylcholine levels fall. This review discusses key genes involved in the pathogenesis and pathophysiology of AD, as well as the disease’s molecular mechanisms.
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