ABSTRACT
DNA damage of neurons is accumulated in Alzheimer's disease (AD). DNA damage-activated Checkpoint kinase 2 (CHEK2) is evaluated in Aß-treated Neuro2a APPSwe/Δ9 cells, and the miR-669b-5p was specifically down-regulated. However, the underlying molecular mechanism between CHEK2 and miR-669b-5p in Neuro2a APPSwe/Δ9 cells remains unclear. This research discovers that in A-treated Neuro2a APPSwe/Δ9 cells, CHEK2 expression and miR-669b-5p expression were inversely correlated. In addition, miR-669b-5p mimics increased cell survival and proliferation in Neuro2a APPSwe/Δ9 cells while decreasing the production of inflammatory cytokines and cell death. Furthermore, it is observed that CHEK2 was a miR-669b-5p downstream target gene and that CHEK2 restored the miR-669b-5p's functions. According to this research, miR-669b-5p is a potential therapy for Alzheimer's patients since it slows the advancement of the disease.
Subject(s)
Alzheimer Disease , MicroRNAs , Humans , Alzheimer Disease/genetics , Alzheimer Disease/metabolism , MicroRNAs/metabolism , Checkpoint Kinase 2/genetics , Checkpoint Kinase 2/metabolism , Neurons/metabolism , Cell Survival , Amyloid beta-Peptides/metabolismABSTRACT
Tuberculosis due to Mycobacterium bovis is a common disease in developing countries, due to its reservoir and most common forms of transmission. Extrapulmonary cases are not uncommon. This fact and the exceptional nature of this mycobacterium, make the diagnosis difficult in our environment. The arrival of migrants from developing countries, where affected cattle and ingestion of contaminated products are frequent, we must be on the alert for an early diagnosis and adequate treatment. We report three cases diagnosed in our region, both with extrapulmonary presentations (cervical lymphadenitis and abdominal tuberculosis), and analyze the present situation of this illness in Spanish livestock, and the influence of immigration on it.
