Alzheimers disease (AD) is a progressive neurodegenerative disorder that deteriorates cognitive function. Patients with AD generally exhibit neuroinflammation, elevated beta-amyloid (Aβ), tau phosphorylation (p-tau), and other pathological changes in the brain. The kynurenine pathway (KP) and several of its metabolites, especially quinolinic acid (QA), are considered to be involved in the neuropathogenesis of AD. The important metabolites and key enzymes show significant importance in neuroinflammation and AD. Meanwhile, the discovery of changed levels of KP metabolites in patients with AD suggests that KP metabolites may have a prominent role in the pathogenesis of AD. Further, some KP metabolites exhibit other effects on the brain, such as oxidative stress regulation and neurotoxicity. Both analogs of the neuroprotective and antineuroinflammation metabolites and small molecule enzyme inhibitors preventing the formation of neurotoxic and neuroinflammation compounds may have potential therapeutic significance. This review focused on the KP metabolites through the relationship of neuroinflammation in AD, significant KP metabolites, and associated molecular mechanisms as well as the utility of these metabolites as biomarkers and therapeutic targets for AD. The objective is to provide references to find biomarkers and therapeutic targets for patients with AD.

As a powerful antioxidant in the human body, uric acid (UA) has been the subject of increasing research that focused on its influence on Alzheimer’s disease (AD) in recent years. The latest literature was gathered to describe the influence of serum uric acid (SUA) level on the onset and progression of AD and to analyze the possibility that SUA is a biomarker of Alzheimer’s disease. A large number of existing studies suggested that the SUA level was lower or tended to decrease in patients with AD, and increased SUA level may have a protective effect in AD, which could reduce the risk of onset and slowing the course of the disease. However, some Mendelian randomization analyses suggested that genetically determined uric acid was not associated with AD risk. Existing research results are contradictory due to the high inconsistency of the studies, the selection of subjects, and other factors. UA also showed a strong association with cognitive function, and there appeared to be a gender‐selective neuroprotective action. Due to its potent antioxidant properties, the low uric acid level may contribute to oxidative stress to accelerate disease progression. But some preclinical data showed a possibility that in some special cases, UA had a prooxidant properties. The possibility was raised in the discussion of the underlying mechanism that both the low uric acid level and the rapidly progressive course of the disease were the consequence of malnutrition. This paper reviews recent advances in the study of SUA and AD which offers the possibility of new biomarker, new prevention, and treatment strategies for Alzheimer’s disease.

Myocardial ischemia-reperfusion injury (MIRI) remains a major clinical challenge, with oxidative stress as a key driver. Despite extensive preclinical promise, antioxidant therapies have consistently failed in clinical translation. This critical review deconstructs this translational gap, which stems from the nuanced complexity of redox biology, inappropriate therapeutic timing, and patient heterogeneity. We argue that overcoming these hurdles requires a paradigm shift from broad antioxidant supplementation to precision medicine. This approach involves enhancing endogenous defense mechanisms, leveraging targeted drug delivery, and developing multi-modal strategies. Ultimately, integrating dynamic biomarkers, multi-omics, and artificial intelligence to tailor treatments to individual patient profiles holds the key to finally fulfilling the promise of effectively managing MIRI.

Purpose: To investigate the effect of sleep disorder (SD) on the changes of brain network dysfunction in mild cognitive impairment (MCI), we compared network connectivity patterns among MCI, SD, and comorbid MCI and sleep disorders (MCI-SD) patients using resting state functional magnetic resonance imaging (RS-fMRI).Patients and Methods: A total of 60 participants were included in this study, 20 each with MCI, SD, or MCI-SD. And all participants underwent structural and functional MRI scanning. The default-mode network (DMN) was extracted by independent component analysis (ICA), and regional functional connectivity strengths were calculated and compared among groups.Results: Compared to MCI patients, The DMN of MCI-SD patients demonstrated weaker functional connectivity with left middle frontal gyrus, right superior marginal gyrus, but stronger connectivity with the left parahippocampus, left precuneus and left middle temporal gyrus. Compared to the SD group, MCI-SD patients demonstrated weaker functional connectivity with right transverse temporal gyrus (Heschl’s gyrus), right precentral gyrus, and left insula, but stronger connectivity with posterior cerebellum, right middle occipital gyrus, and left precuneus.Conclusion: Patients with MCI-SD show unique changes in brain network connectivity patterns compared to MCI or SD alone, likely reflecting a broader functional disconnection and the need to recruit more brain regions for functional compensation.