Potential Health Risks Associated with Sports Supplementation Use in Athletes.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. As the disease progresses, cognitive capabilities gradually deteriorate, with memory impairment and diminished learning ability []. Amid the global increase in the elderly population, AD has emerged as a major and unignorable public-health concern. With over 50 million people worldwide affected by this condition, it imposes not only significant burdens on family caretakers but also substantial challenges on society as a whole [,]. Clinical features of AD are the accumulation of amyloid-β plaques and the presence of neurofibrillary tangles in the cerebral cortex—essentially abnormal clusters of hyperphosphorylated tau protein []. Recently conducted investigations have revealed the intricacies of the pathogenic processes underlying AD, which comprise a series of events—including neuroinflammation, redox-mediated oxidative damage, disruption of mitochondrial metabolism, impaired autophagy, endoplasmic reticulum protein misfolding, and others []. Although scientists have devoted considerable effort to studying these disease-related pathways, when it comes to daily clinical practice, we still lack drugs that can truly alter the course of the disease and offer what could be described as a “root-cause” cure. The GBA acts as a multi-directional signaling hub connecting the enteric microbiota to the CNS via neural, immuno-endocrine, and metabolic-endocrine pathways [,]. In years past, a surge of studies confirmed this axis’s pivotal role in modulating AD pathogenesis, paving the way for novel future therapeutic development [,]. Notably, numerous clinical studies and animal experiments have revealed that the gut microbiota of AD patients is significantly disrupted—a condition known as dysbiosis. Messages communicated through the microbiota-gut–brain axis (MGBA) signaling pathway further influence the core aspects of this disorder, encompassing β-amyloid deposits, tau phosphorylation, and brain inflammation []. When viewed collectively, the findings provide a firm theoretical basis for the notion that regulating the gut microbiota could serve as a potential therapeutic approach for AD []. In TCM, herbs rich in polysaccharides have actually been used for a very long time. In ancient times, they were said to “tonify qi,” “enhance intelligence,” and “nourish the brain [,].” Current pharmacological research confirms that polysaccharides extracted from Chinese herbs improve cognitive deficits primarily through two mechanisms: first, by suppressing inflammatory responses in the brain, and second, by modulating the composition of the gut microbiota []. Interestingly, these polysaccharides are typically regarded as having a low gut absorption rate and difficulty traversing the BBB; nevertheless, their significant neuroprotective function in the central neuroaxis has been well-established []. This apparent contradiction is explained by the gut microbiota: through regulating microbial metabolites, polysaccharides modulate brain function [,]. Recent studies have also confirmed that the gut microbiota plays a key mediating role in regulating the gut–brain axis and influencing neurodegenerative diseases. This explains why naturally derived bioactive compounds can exert neuroprotective effects via this axis []. Overall, this line of reasoning not only provides a solid pharmacological basis for using polysaccharides from TCM to combat AD but also charts a new path for the modernization of TCM and the discovery of new drugs. This review, therefore, bridges phytochemical characterization of polysaccharides with their gut microbiota-driven molecular mechanisms, offering an integrated framework that resolves the long-standing PK–PD paradox and highlights therapeutic opportunities for AD. The literature covers the period from 2010 to 2026, with emphasis on studies of the structural features, microbiota-mediated metabolism, and neuroprotective mechanisms of TCM polysaccharides in AD models.