The role of non-coding RNA-mediated autophagy in Alzheimer’s disease

Apr 4, 2026Brain research bulletin

How Non-Coding RNA May Influence Cell Cleanup Processes in Alzheimer's Disease

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Abstract

Dysfunctional autophagy is implicated in the pathogenesis of Alzheimer's disease.

Alzheimer's disease is a major cause of dementia, affecting patients and healthcare systems globally.
Autophagy is essential for removing damaged cellular components and maintaining metabolic balance.
Non-coding RNAs, including microRNAs, long ncRNAs, and circular RNAs, regulate autophagy and influence Alzheimer's disease progression.
Targeting the interaction between non-coding RNAs and autophagy may offer new therapeutic strategies for Alzheimer's disease.

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder and one of the leading causes of dementia, imposing a profound burden on patients, families, and healthcare systems worldwide. Autophagy, an evolutionarily conserved lysosomal degradation pathway critical for maintaining cellular homeostasis, removes damaged organelles and misfolded proteins, thereby preserving metabolic balance and enabling intracellular biomolecule recycling. Growing evidence indicates that dysfunctional autophagy contributes to AD pathogenesis. Concurrently, non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), have emerged as pivotal regulators of AD pathology, particularly through mechanisms involving autophagy. These ncRNAs not only play a role in disease progression but also represent promising molecular targets for therapeutic intervention via autophagy modulation. This review systematically explores the regulatory networks through which ncRNAs influence autophagy in AD, with the goal of identifying potential therapeutic targets and offering a conceptual framework to guide clinical translation.

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The role of non-coding RNA-mediated autophagy in Alzheimer’s disease

Abstract

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