Background: Alzheimer’s disease (AD) is the most common form of dementia. AD is also the leading cause of morbidity and mortality due to dementia worldwide. It has been shown that AD is associated with type 2 diabetes mellitus (T2DM) and brain insulin resistance. Rs1801278 is a polymorphism in insulin receptor substrate-1 (IRS-1) gene which changes the amino acid Arg972. This polymorphism has been found to be associated with susceptibility to AD in some populations. Objective: In the present study, our aim was to investigate the association of Arg972 IRS-1 (rs1801278) gene polymorphism and late-onset Alzheimer’s disease (LOAD) in an Iranian population. Methods: In this case-control study, 150 patients with LOAD and 150 unrelated healthy controls were recruited. Polymerase chain reaction (PCR) was performed to amplify a DNA segment of 263 base-pair (bp) length containing the single nucleotide polymorphism (SNP). The PCR product was then incubated with MvaI restriction enzyme to undergo enzymatic cleavage. Electrophoresis was thereafter carried out using agarose gel and DNA safe stain. The gel was ultimately visualized under a UV trans-illuminator. Allelic and genotypic frequencies were then compared. Results: A allele (mutant) of the gene was significantly associated with the risk of AD after adjustment for sex and age (p = 0.04, adjusted OR:1.77, 95% CI:1.00–3.11). Only AA genotype (mutant homozygote) was significantly associated with the risk of AD after adjustment for sex and age (p = 0.01, adjusted OR:2.39, 95% CI:1.22–4.66). Conclusion: SNP rs1801278 is significantly associated with the risk of developing AD in the studied Iranian population.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak became one of the most global health challenges in the recent century. Transverse myelitis is a rare medical condition reported in few case reports following COVID-19 infection. We present a 63 years old female with post-COVID-19 transverse myelitis. The patient had paraplegia combined with autonomic symptoms and T4 sensory level. Initial treatment started with methylprednisolone. Since the patient did not respond to the prednisolone, plasmapheresis was considered for the patient. Unfortunately, the patient could not tolerate the plasmapheresis. We considered rituximab for the next plan, but unfortunately, the patient died due to respiratory failure. To date, there is no published study to evaluate different mechanisms of post/para COVID-19 transverse myelitis. However, the post/para COVID-19 transverse myelitis mechanism seems to be heterogeneous; the activation of a silent autoimmune disease can probably justify some unusual clinical presentations of a viral illness. Further studies are needed to categorize the underlying mechanisms of post/para COVID-19 transverse myelitis and effective treatments regarding the primary pathology.
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