**Background:** Neurological diseases of the central nervous system represent a growing global health burden, with the WHO projecting unipolar depression to overtake major oncological and metabolic diseases by 2030. The European Brain Council estimates that one in three Europeans suffers from a brain disorder annually. Neurological conditions are increasingly linked to oxidative stress, inflammation, and lifestyle factors including diet. This narrative review examines the role of diet as a modulator of inflammation in neurological disease development and progression.
**Methods:** The authors conducted a narrative review of the published literature, synthesizing evidence from randomized controlled trials, prospective cohort studies, meta-analyses, and preclinical studies examining dietary interventions and their effects on inflammatory markers and neurological outcomes. The review covers multiple dietary patterns including the Mediterranean diet, ketogenic diet, DASH diet, anti-inflammatory diet, and very low-calorie ketogenic diets. It also examines specific dietary components including fruits, vegetables, herbs, spices, omega-3 fatty acids, probiotics, and individual bioactive compounds.
**Key Results:** The review presents data from multiple clinical studies. In Alzheimer's disease, a 12-week randomized trial by Akbari et al. (2008) of 80 patients found that a ketogenic diet produced significant improvements in cognitive function (Mini-Mental State Examination) and reductions in IL-6 and TNF-alpha compared to usual diet. Phillips et al. (2018) demonstrated that AD patients on a ketogenic diet achieved sustained physiological ketosis (mean beta-hydroxybutyrate 0.95±0.34 mmol/L over 12 weeks) with improvements in ADCS-ADL (+3.13±5.01) and QOL-AD (+3.37±6.86). In Parkinson's disease, Paknahad et al. (2020) showed in 80 patients that a Mediterranean diet over 3 months produced significant reductions in inflammatory markers and improvements in Unified Parkinson's Disease Rating Scale scores. A ketogenic diet study by Phillips et al. (2018) in 44 PD patients over 8 weeks showed greater improvements in nonmotor symptoms compared to a low-fat diet. In multiple sclerosis, Mousavi-Shirazi-Fard et al. (2021) demonstrated in 100 patients that a 12-week anti-inflammatory diet significantly increased IL-4 levels and improved Modified Fatigue Impact Scale and MSQoL-54 scores. For depression, Lai et al. (2014) found that a DASH diet reduced depression severity and anxiety scores with lower levels of CRP, IL-6, and TNF-alpha. Shivappa et al. reported that individuals with a pro-inflammatory diet had a 24% higher risk of developing depressive symptoms over 8 years. In schizophrenia, Jahrami et al. confirmed a positive correlation between Dietary Inflammatory Index scores and schizophrenia. The review also documents that gut microbiome alterations are observed across neurological conditions, with reduced beneficial bacteria (Prevotella, Bifidobacterium, Lactobacillus) and increased pro-inflammatory bacteria (Collinsella, Escherichia coli, Enterobacteriaceae) in MS, AD, PD, and depression.
**Clinical Implications:** The evidence supports that dietary interventions can serve as non-invasive, practical adjunctive strategies for managing neurological disorders. Anti-inflammatory dietary patterns—particularly the Mediterranean diet, ketogenic diet, and DASH diet—show promise in reducing inflammatory markers, improving cognitive function, and enhancing quality of life across multiple neurological conditions. The gut-brain axis emerges as a critical pathway through which diet influences neurological health, with probiotics and prebiotics showing potential as supplementary treatments. The Dietary Inflammatory Index provides a validated tool for assessing dietary inflammatory potential. However, the authors note that most studies have small sample sizes and short durations, and the heterogeneity of neurological conditions suggests that personalized nutritional approaches may be more effective than one-size-fits-all interventions. Further research is needed to elucidate the mechanisms by which dietary components influence neurological disease etiology and progression.