International journal of biological macromoleculesAug 28, 2026

Polysaccharides that may improve organelle network problems in Alzheimer's disease

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Aug 29, 2026

Abstract

Alzheimer's disease pathology may involve a core organelle network amplifying oxidative stress and neuroinflammation.

Dysfunction and interaction among mitochondria, endoplasmic reticulum, and lysosome-autophagy contribute to Alzheimer's disease progression.
Polysaccharides could serve as multitarget modulators influencing organelle-associated pathways related to Alzheimer's dysfunction.
Structural properties of polysaccharides, such as molecular weight and composition, are associated with their bioactivities in signaling pathways and inflammation regulation.
Rational design strategies for polysaccharides may enhance their efficacy and readiness for clinical application.
Challenges such as heterogeneity and brain delivery need to be addressed for effective polysaccharide-based interventions in Alzheimer's.

Simplified

Alzheimer's disease (AD) is driven by an interrelated pathological network, which to some extent explains the limited efficacy of single-target therapies and constitutes a significant challenge in current clinical treatment. Emerging evidence indicates that dysfunction and crosstalk among mitochondria, the endoplasmic reticulum, and lysosome-autophagy form a core organelle network that amplifies oxidative stress and exacerbates proteostatic imbalance, neuroinflammation, and synaptic failure. In this review, we summarize natural and engineered polysaccharides as potential multitarget modulators that may influence individual organelle-associated pathways involved in AD-related dysfunction. We discuss how the structural parameters of polysaccharides (e.g., molecular weight, monosaccharide composition, glycosidic linkages, branching, and charge density) are associated with bioactivities through receptor-related signaling pathways, redox and inflammatory regulation, proteostasis/autophagy modulation, and, when applicable, potential gut-brain axis involvement. Furthermore, we highlight rational design strategies (e.g., sulfation and carboxymethylation) and formulation/delivery considerations that may increase efficacy and translational readiness. Finally, key challenges, including heterogeneity, mechanism attribution, brain delivery, and standardization, are outlined to guide the development of polysaccharide-based strategies potentially addressing organelle-associated dysfunction in AD.

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Polysaccharides that may improve organelle network problems in Alzheimer's disease

Abstract

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