How do energy metabolism disorders and neuroinflammation collectively contribute to the pathogenesis of Alzheimer's disease?

Neuroinflammatory and molecular pathways in Alzheimer’s disease: mechanistic crosstalk and emerging therapeutic opportunities

Overall, this review makes a case for integrative, pathway-based therapeutic models, and multiple approaches may facilitate for drug development, biomarker identification and patient management in Alzheimer's disease.

Oxidative Stress in Alzheimer’s Disease: Can Dietary Interventions Provide Neuroprotection?

Population aging is a growing problem. This process is driven not only by genetic factors but also by environmental factors, such as diet. Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, characterized by cognitive decline, synaptic dysfunction, and neuronal loss. Despite extensive research, effective disease-modifying therapies remain limited. Increasing evidence indicates that oxidative stress plays a central role in AD pathogenesis, acting as a key link between β-amyloid accumulation, tau hyperphosphorylation, mitochondrial dysfunction, and neuroinflammation. Accordingly, dietary strategies have been proposed to mitigate these pathological processes and may represent an important component of Alzheimer’s disease prevention. Moreover, emerging evidence on the gut–brain axis highlights the critical role of gut microbiota in regulating neuroinflammation and oxidative stress. Dysbiosis has been associated with increased permeability of the intestinal barrier, systemic inflammation, and accelerated neurodegeneration. Dietary patterns such as the Mediterranean, DASH, and MIND diets may exert beneficial effects by simultaneously influencing antioxidant status and microbial composition. This review aims to provide a comprehensive overview of the role of oxidative stress in Alzheimer’s disease and evaluate the potential of dietary interventions in modulating mechanisms involved in Alzheimer’s disease pathogenesis and supporting cognitive health. Particular attention is given to the neuroprotective effects of dietary antioxidants, including vitamins, polyphenols, and polyunsaturated fatty acids, which act through the reduction in reactive oxygen species, modulation of inflammatory pathways, and support of neuronal survival. Although current findings are promising, inconsistencies in clinical data indicate the need for further well-designed studies. Future research should focus on personalized nutritional strategies integrating dietary, genetic, and microbiome-related factors. Targeting oxidative stress through diet and microbiota modulation represents a promising complementary strategy for Alzheimer’s disease prevention and supportive management, although further clinical studies are required to establish disease-modifying effects.

Metabolic drivers of Alzheimer's disease pathogenesis: Impairments in glucose utilization, lipid homeostasis, and alternative substrate metabolism.

Metabolic therapeutic targets in Alzheimer's disease.

Therapeutic targeting of brain bioenergetics in Alzheimer's disease addressing insulin resistance, glucose hypometabolism, and mitochondrial dysfunction.

Mechanisms, Biomarkers and Therapeutic Implications of Neuroinflammation in Alzheimer's Disease

The dual and stage‐dependent roles of microglia and astrocytes are explored, discussion of blood–brain barrier dysfunction and peripheral immune infiltration as underappreciated pathogenic contributors are expanded, and emerging evidence linking neuroinflammation specifically to tau pathology is integrated.