Differential Expression and miRNA–Gene Interactions in Early and Late Mild Cognitive Impairment

Brito, Leonardo Miranda; Ribeiro-dos-Santos, Ândrea; Vidal, Amanda Ferreira; Araújo, Gilderlanio Santana de

doi:10.3390/biology9090251

Cited by 24 publications

(16 citation statements)

References 51 publications

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“…Dysregulation of calcium homeostasis, an intrinsic ionic regulator, plays a critical role in the initiation and progression of AD as the calcium binding protein calmodulin, and the calmodulin binding protein neurogranin, are reported to be involved in AD associated long-term depression. Calmodulin inhibitors improved cognitive functions in an animal model of vascular dementia [40,41]. Further, disturbed calcium homeostasis induced increased intracellular calcium and calmodulin leads to activation of NMDA and AMPA receptors, responsible for long term depression associated with AD [40].…”

Section: Discussionmentioning

confidence: 99%

Sinapic Acid Alleviates Oxidative Stress and Neuro-Inflammatory Changes in Sporadic Model of Alzheimer’s Disease in Rats

Verma

Singh

2020

Brain Sciences

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The role of oxidative stress, neuro-inflammation and cholinergic dysfunction is already established in the development of Alzheimer’s disease (AD). Sinapic acid (SA), a hydroxylcinnamic acid derivative, has shown neuro-protective effects. The current study evaluates the neuro-protective potential of SA in intracerebroventricular streptozotocin (ICV-STZ) induced cognitive impairment in rats. Male Wistar rats were bilaterally injected with ICV-STZ. SA was administered intragastrically once daily for three weeks. Rats were divided into sham, ICV-STZ, STZ + SA (10 mg/kg), STZ + SA (20 mg/kg) and SA per se (20 mg/kg). Behavioral tests were assessed on day 0 and 21 days after STZ. Later, rats were sacrificed for biochemical parameters, pro-inflammatory cytokines, choline acetyltransferase (ChAT) expression and neuronal loss in the CA1 region of the hippocampus. The results showed that SA 20 mg/kg significantly (p < 0.05) improved cognitive impairment as assessed by Morris water maze and passive avoidance tests. SA 20 mg/kg reinstated the altered levels of GSH, MDA, TNF-α and IL-1β in the cortex and hippocampus. STZ-induced decreased expression of ChAT and neuronal loss were also significantly (p < 0.05) improved with SA. Our results showed that SA exhibits neuro-protection against ICV-STZ induced oxidative stress, neuro-inflammation, cholinergic dysfunction and neuronal loss, suggesting its potential in improving learning and memory in patients of AD.

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Section: Discussionmentioning

confidence: 99%

Sinapic Acid Alleviates Oxidative Stress and Neuro-Inflammatory Changes in Sporadic Model of Alzheimer’s Disease in Rats

Verma

Singh

2020

Brain Sciences

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“…Alzheimer's disease (AD) is the most common form of neurodegenerative disease [1,2]. AD patients usually experience a progressive loss of cognitive function, memory, and intellectual activity [2,3]. Amyloid-β (Aβ) peptide plays an important role in AD pathogenesis and is the main component of senile plaques [2,4,5].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanism of Vitamin K2 Protection against Amyloid-β-Induced Cytotoxicity

2021

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The pathological role of vitamin K2 in Alzheimer’s disease (AD) involves a definite link between impaired cognitive functions and decreased serum vitamin K levels. Vitamin K2 supplementation may have a protective effect on AD. However, the mechanism underlying vitamin K2 protection has not been elucidated. With the amyloid-β (Aβ) cascade hypothesis, we constructed a clone containing the C-terminal fragment of amyloid precursor protein (β-CTF/APP), transfected in astroglioma C6 cells and used this cell model (β-CTF/C6) to study the protective effect of vitamin K2 against Aβ cytotoxicity. Both cellular and biochemical assays, including cell viability and reactive oxygen species (ROS), assays assay, and Western blot and caspase activity analyses, were used to characterize and unveil the protective role and mechanism of vitamin K2 protecting against Aβ-induced cytotoxicity. Vitamin K2 treatment dose-dependently decreased the death of neural cells. The protective effect of vitamin K2 could be abolished by adding warfarin, a vitamin K2 antagonist. The addition of vitamin K2 reduced the ROS formation and inhibited the caspase-3 mediated apoptosis induced by Aβ peptides, indicating that the mechanism underlying the vitamin K2 protection is likely against Aβ-mediated apoptosis. Inhibitor assay and Western blot analyses revealed that the possible mechanism of vitamin K2 protection against Aβ-mediated apoptosis might be via regulating phosphatidylinositol 3-kinase (PI3K) associated-signaling pathway and inhibiting caspase-3-mediated apoptosis. Our study demonstrates that vitamin K2 can protect neural cells against Aβ toxicity.

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“…miRNAs are short non-coding RNAs responsible for gene expression at the post-transcriptional level. Altered miRNAs have been linked to mitochondrial dysfunction and oxidative stress in ageing and neurodegenerative diseases [54]. miR-133b, miR-7, miR153, miR-433, miR-433, miR-205, and miR-124 are of interest as possible biomarkers in PD [55].…”

Section: Discussionmentioning

confidence: 99%

Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase Influenced the Age Onset of Parkinson’s Disease

Török¹,

Maszlag-Török²,

Molnár³

et al. 2021

Preprint

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Aims Earlier studies reported alterations of the kynurenine (KYN) pathway of tryptophan (TRP) metabolism in Parkinson’s disease (PD). The first rate-limiting enzymes indoleamine 2,3- dioxygenase (IDO) and tryptophan dioxygenase were observed upregulated, resulting elevated KYN/TRP ratios in the serum and cerebrospinal fluid samples of patients with PD. An increasing number of single nucleotide polymorphisms (SNPs) has been identified in a population of PD. However, little is known if genetic variations of the IDO contribute to disturbance of the KYN metabolism in and the pathogenesis of PD. Main methods SNP analysis of IDO1 was performed by allelic discrimination assay with fluorescently labelled TaqMan probes and a subgroup analysis was conducted according to the age of PD onset. The frame shifts variant rs34155785, intronic variant rs7820268, and promotor region variant rs9657182 SNPs of 105 PD patients without comorbidity were analyzed and compared to 129 healthy controls. Key findings No significant correlation was found in three SNPs between PD patients and healthy controls. However, the subgroup analysis revealed that A alleles of rs7820268 SNP or rs9657182 SNP carriers contribute to later onset of PD than non-carriers. Significance The study suggested that SNPs of IDO1 influenced the age onset of PD and genotyping of SNPs in certain alleles potentially serves as a risk biomarker of PD.

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Differential Expression and miRNA–Gene Interactions in Early and Late Mild Cognitive Impairment

Cited by 24 publications

References 51 publications

Sinapic Acid Alleviates Oxidative Stress and Neuro-Inflammatory Changes in Sporadic Model of Alzheimer’s Disease in Rats

Sinapic Acid Alleviates Oxidative Stress and Neuro-Inflammatory Changes in Sporadic Model of Alzheimer’s Disease in Rats

Molecular Mechanism of Vitamin K2 Protection against Amyloid-β-Induced Cytotoxicity

Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase Influenced the Age Onset of Parkinson’s Disease

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