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.
Abstract
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.
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive dysfunction. Docosahexaenoic acid (DHA), the most abundant ω-3 polyunsaturated fatty acid (PUFA) in the brain, is essential for neuronal structure and function. Although epidemiological studies generally associate higher DHA...
Xin-Hua Li, Yue Jin, Xiao-Yu Li et al.· Pharmacological Research· 0 citations
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.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder whose pathological course involves amyloid-β (Aβ) deposition, tau abnormalities, neuroinflammation, and neurovascular dysfunction. Interest in the microbiota-gut-brain axis does not arise because gut dysbiosis has been established as an independent in...
Jing-Yi Wang, Lyu Luo, Jiawang Zhang et al.· Ageing Research Reviews· 0 citations
This review systematically elaborates the potential molecular mechanisms through which KD protects against PD, which covers the improvement of cerebral energy metabolism, antioxidant and anti-apoptotic activities, suppression of neuroinflammation, regulation of α-synuclein pathological aggregation, and modulation of gu...
Mula A, Yan Bai, Yu-Lin Wang et al.· Frontiers in Nutrition· 0 citations
Background: Alzheimer’s Disease (AD) is the most prevalent neurodegenerative disorder and a leading cause of dementia, involving the gradual loss of cognitive function, memory, and neurons. While the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs), caused by hyperphosphorylation of the protein...
This review examines the molecular and cellular mechanisms through which neuroinflammation contributes to the progression of AD, with particular emphasis on microglial activation, TREM2 and soluble TREM2 (sTREM2) signaling, NLRP3 inflammasome activation, astrocyte–microglia interactions, and blood–brain barrier dysfunc...
Shreyansh Goswami· International Journal For Mu...· 0 citations
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