review · International Journal of Molecular Sciences
Alzheimer's disease is a progressive neurodegenerative condition that causes memory and cognitive decline, characterised by amyloid-beta plaques and tau protein tangles that drive neuroinflammation, oxidative stress, and synaptic dysfunction. While onset is influenced by genetic, epigenetic, behavioural, and environmental factors, variations in non-coding RNAs are also strongly implicated in disease mechanisms. This review examines alterations across several classes of non-coding molecules, including circular RNA, microRNA, short interfering RNA, piwi-interacting RNA, and long non-coding RNA. These molecular changes present opportunities to develop diagnostic biomarkers and therapeutic targets for Alzheimer's disease. Furthermore, evaluating studies that target non-coding RNAs in cellular and animal models highlights pathways for translating laboratory findings into potential disease treatments.
Alzheimer's disease causes profound cognitive loss, yet effective diagnostic and therapeutic options remain limited. Uncovering how non-coding RNAs contribute to cellular dysfunction helps clarify the multi-faceted mechanisms of disease onset and progression. This understanding highlights biological targets that could guide the development of earlier diagnostic tools and new medical treatments for neurodegenerative disorders.
This research points towards applications in diagnostic biomarker discovery and therapeutic development for Alzheimer's disease, targeting pharmaceutical and biotechnology developers. Given that the evaluated interventions rely on cellular and animal models, the technology remains at an early preclinical stage and requires significant further development before reaching clinical or market use.
AI-generated from the published abstract. Always read the original work before citing.
Alzheimer's disease (AD) is a chronic neurodegenerative disorder that is accompanied by deficits in memory and cognitive functions. The disease is pathologically characterised by the accumulation and aggregation of an extracellular peptide referred to as amyloid-β (Aβ) in the form of amyloid plaques and the intracellular aggregation of a hyperphosphorelated protein tau in the form of neurofibrillary tangles (NFTs) that cause neuroinflammation, synaptic dysfunction, and oxidative stress. The search for pathomechanisms leading to disease onset and progression has identified many key players that include genetic, epigenetic, behavioural, and environmental factors, which lend support to the fact that this is a multi-faceted disease where failure in various systems contributes to disease onset and progression. Although the vast majority of individuals present with the sporadic (non-genetic) form of the disease, dysfunctions in numerous protein-coding and non-coding genes have been implicated in mechanisms contributing to the disease. Recent studies have provided strong evidence for the association of non-coding RNAs (ncRNAs) with AD. In this review, we highlight the current findings on changes observed in circular RNA (circRNA), microRNA (miRNA), short interfering RNA (siRNA), piwi-interacting RNA (piRNA), and long non-coding RNA (lncRNA) in AD. Variations in these ncRNAs could potentially serve as biomarkers or therapeutic targets for the diagnosis and treatment of Alzheimer's disease. We also discuss the results of studies that have targeted these ncRNAs in cellular and animal models of AD with a view for translating these findings into therapies for Alzheimer's disease.
This page summarises published work. The authoritative version sits with the publisher.
DOI: 10.3390/ijms241512498
Is something wrong with this record? Report it or request removal.
Discussion
Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.
No discussion yet. Open the first thread.
New to MARATTO™? Create a free account.
