Cerebral Amyloid Angiopathy, Alzheimer ’s Disease and MicroRNA: miRNA as Diagnostic Biomarkers and Potential Therapeutic Targets
AbstractThe protein molecules must fold into unique conformations to acquire functional activity. Misfolding, aggregation, and deposition of proteins in diverse organs, the so-called “protein misfolding disorders (PMDs)”, represent the conformational diseases with highly ordered assemblies, including oligomers and fibrils that are linked to neurodegeneration in brain illnesses such as cerebral amyloid angiopathy (CAA) and Alzheimer’s disease (AD). Recent studies have revea led several aspects of brain pathology in CAA and AD, but both the classification and underlying mechanisms need to be further refined. MicroRNAs (miRNAs) are critical regulators of gene expression at the post-transcriptional level. Increasing evidence with the advent of RNA sequencing technology suggests possible links between miRNAs and these neurodegenerative disorders. To provide insights on the small RNA-mediated regulatory circuitry and the translational significance of miRNAs in PMDs, this review will discuss the characteristics and mechanisms of the diseases and summarize circulating or tissue-resident miRNAs associated with AD and CAA.
Chem. Commun., 2020, Accepted Manuscript DOI: 10.1039/D0CC01551B, Feature ArticleBikash Sahoo, Sarah N Cox, Ayyalusamy Ramamoorthy In Alzheimer ’s disease (AD), soluble oligomers of amyloid-β (Aβ) are emerging as a crucial entity in driving disease progression as compared to insoluble amyloid deposits. The lacuna in establishing the... The content of this RSS Feed (c) The Royal Society of Chemistry
Conclusion: ART may reduce the risk of NCIs in HIV-infected patients in general. Further research to investigate NCIs on specific antiretroviral regimens and comorbidities may provide insights regarding the long-term clinical care of these patients.
Conclusions/interpretationOur findings suggest positive associations of plasma A β40 and Aβ42 concentration with risk of type 2 diabetes. Further studies are warranted to elucidate the underlying mechanisms and explore the potential roles of plasma Aβ in linking type 2 diabetes and Alzheimer’s disease.
Publication date: Available online 9 April 2020Source: Journal of EthnopharmacologyAuthor(s): Yi Chen, Ying-Qi Li, Jia-Yi Fang, Ping Li, Fei Li
Condition: Alzheimer Disease Intervention: Drug: Gantenerumab Sponsor: Hoffmann-La Roche Not yet recruiting
Conclusions: These findings indicated that the administration of Hst and Nano-Hst may be used to treat anxiety -related to AD via an up-regulation of cerebral antioxidant enzyme gene. PMID: 32252616 [PubMed - as supplied by publisher]
OBJECTIVES: To examine the driving variables that predict accident probability in mild dementia due to Alzheimer's disease (AD), mild cognitive impairment (MCI) and healthy older control drivers in simulated driving. To compare the three groups in mean per...
In this study, we have investigated the role of all-trans-retinoic acid (RA) as a neuroprotective agent against Aβ 1-42-induced DNA double-strand breaks (DSBs) in neuronal SH-SY5Y and astrocytic DI TNC1 cell lines and in murine brain tissues, by single-cell gel electrophoresis. We showed that RA does not only repair Aβ 1-42-induced DSBs, as already known, but also prevents their occurrence. This effect is independent of that of other antioxidants studied, such as vitamin C, and appears to be mediated, at least in part, by changes in expression, not of the RARα, but of the PPARβ/δ and of antiamylo...
This study suggests that exercise improves cognition and neural activity by altering the numbers and distribution of hippocampal Nav in APP/PS1 mice. Long-term treadmill exercise, for about 24 weeks, starting in the preclinical stage, is a promising therapeutic strategy for preventing AD and halting its progress. PMID: 32256560 [PubMed - as supplied by publisher]
Calpains represent a family of calcium-dependent proteases participating in a multitude of functions under physiological or pathological conditions. Calpain-1 is one of the most studied members of the family, is ubiquitously distributed in organs and tissues, and has been shown to be involved in synaptic plasticity and neuroprotection in mammalian brain. Calpain-1 deletion results in a number of phenotypic alterations. While some of these alterations can be explained by the acute functions of calpain-1, the present study was directed at studying alterations in gene expression that could also account for these phenotypic mo...