An Anti-Inflammatory Diet and Its Potential Benefit for Individuals with Mental Disorders and Neurodegenerative Diseases-A Narrative Review.

This narrative review synthesizes current evidence regarding anti-inflammatory dietary patterns and their potential benefits for individuals with mental disorders and neurodegenerative diseases. Chronic low-grade inflammation is increasingly recognized as a key factor in the etiology and progression of these conditions. The review examines the evidence for the anti-inflammatory and neuroprotective properties of dietary components and food groups, focusing on whole foods rather than specific nutrients or supplements. Key dietary components showing potential benefits include fruits and vegetables (especially berries and leafy greens), whole grains, legumes, fatty fish rich in omega-3, nuts (particularly walnuts), olive oil, and fermented foods. These foods are generally rich in antioxidants, dietary fiber, and bioactive compounds that may help modulate inflammation, support gut health, and promote neuroprotection. Conversely, ultra-processed foods, red meat, and sugary beverages may be harmful. Based on this evidence, we designed the Brain Anti-Inflammatory Nutrition (BrAIN) diet. The mechanisms of this diet include the modulation of the gut microbiota and the gut-brain axis, the regulation of inflammatory pathways, a reduction in oxidative stress, and the promotion of neuroplasticity. The BrAIN diet shows promise as an aid to manage mental and neurodegenerative disorders.

Shared effects of electroconvulsive shocks and ketamine on neuroplasticity: A systematic review of animal models of depression.

Electroconvulsive shocks (ECS) and ketamine are antidepressant treatments with a relatively fast onset of therapeutic effects compared to conventional medication and psychotherapy. While the exact neurobiological mechanisms underlying the antidepressant response of ECS and ketamine are unknown, both interventions are associated with neuroplasticity. Restoration of neuroplasticity may be a shared mechanism underlying the antidepressant efficacy of these interventions. In this systematic review, literature of animal models of depression is summarized to examine the possible role of neuroplasticity in ECS and ketamine on a molecular, neuronal, synaptic and functional level, and specifically to what extent these mechanisms are shared between both interventions. The results highlight that hippocampal neurogenesis and brain-derived neurotrophic factor (BDNF) levels are consistently increased after ECS and ketamine. Moreover, both interventions positively affect glutamatergic neurotransmission, astrocyte and neuronal morphology, synaptic density, vasculature and functional plasticity. However, a small number of studies investigated these processes after ECS. Understanding the shared fundamental mechanisms of fast-acting antidepressants can contribute to the development of novel therapeutic approaches for patients with severe depression.

Changes in perfusion, and structure of hippocampal subfields related to cognitive impairment after ECT: A pilot study using ultra high field MRI.

BACKGROUND: Electroconvulsive therapy (ECT) in patients with major depression is associated with volume changes and markers of neuroplasticity in the hippocampus, in particular in the dentate gyrus. It is unclear if these changes are associated with cognitive side effects. OBJECTIVES: We investigated whether changes in cognitive functioning after ECT were associated with hippocampal structural changes. It was hypothesized that 1) volume increase of hippocampal subfields and 2) changes in perfusion and diffusion of the hippocampus correlated with cognitive decline. METHODS: Using ultra high field (7 T) MRI, intravoxel incoherent motion and volumetric data were acquired and neurocognitive functioning was assessed before and after ECT in 23 patients with major depression. Repeated measures correlation analysis was used to examine the relation between cognitive functioning and structural characteristics of the hippocampus. RESULTS: Left hippocampal volume, left and right dentate gyrus and right CA1 volume increase correlated with decreases in verbal memory functioning. In addition, a decrease of mean diffusivity in the left hippocampus correlated with a decrease in letter fluency. LIMITATIONS: Due to methodological restrictions direct study of neuroplasticity is not possible. MRI is used as an indirect measure. CONCLUSION: As both volume increase in the hippocampus and MD decrease can be interpreted as indirect markers for neuroplasticity that co-occur with a decrease in cognitive functioning, our results may indicate that neuroplastic processes are affecting cognitive processes after ECT.

Unhealthy diet in schizophrenia spectrum disorders.

PURPOSE OF REVIEW: The high mortality and prevalence of metabolic syndrome in patients with schizophrenia spectrum disorders (SSD) is maintained by poor diet. This narrative review summarizes recent literature to provide a reflection of current eating habits, dietary preferences, and nutritional status of SSD patients. Elucidating these factors provides new insights for potential lifestyle treatment strategies for SSD. RECENT FINDINGS: Only 10.7% of the SSD patients had a healthy dietary pattern, against 23% of the general population. The dietic component of the Keeping the Body in Mind Xtend lifestyle program increased diet quality with 10% for young people with first-episode psychosis, compared to baseline, which was predominantly driven by increased vegetable variety and amounts. SUMMARY: Recent findings render poor dietary habits as potential targets for treatment of SSD patients. Further studies into anti-inflammatory diets and associations with gut-brain biomarkers are warranted. When proven, structured and supervised diet interventions may help SSD patients escape from this entrapment, as only supplementing nutrients or providing dietary advice lacks the impact to significantly reduce the risk of chronic physical illnesses.

Interrogating Associations Between Polygenic Liabilities and Electroconvulsive Therapy Effectiveness.

BACKGROUND: Electroconvulsive therapy (ECT) is the most effective treatment for severe major depressive episodes (MDEs). Nonetheless, firmly established associations between ECT outcomes and biological variables are currently lacking. Polygenic risk scores (PRSs) carry clinical potential, but associations with treatment response in psychiatry are seldom reported. Here, we examined whether PRSs for major depressive disorder, schizophrenia (SCZ), cross-disorder, and pharmacological antidepressant response are associated with ECT effectiveness. METHODS: A total of 288 patients with MDE from 3 countries were included. The main outcome was a change in the 17-item Hamilton Depression Rating Scale scores from before to after ECT treatment. Secondary outcomes were response and remission. Regression analyses with PRSs as independent variables and several covariates were performed. Explained variance (R2) at the optimal p-value threshold is reported. RESULTS: In the 266 subjects passing quality control, the PRS-SCZ was positively associated with a larger Hamilton Depression Rating Scale decrease in linear regression (optimal p-value threshold = .05, R2 = 6.94%, p < .0001), which was consistent across countries: Ireland (R2 = 8.18%, p = .0013), Belgium (R2 = 6.83%, p = .016), and the Netherlands (R2 = 7.92%, p = .0077). The PRS-SCZ was also positively associated with remission (R2 = 4.63%, p = .0018). Sensitivity and subgroup analyses, including in MDE without psychotic features (R2 = 4.42%, p = .0024) and unipolar MDE only (R2 = 9.08%, p < .0001), confirmed the results. The other PRSs were not associated with a change in the Hamilton Depression Rating Scale score at the predefined Bonferroni-corrected significance threshold. CONCLUSIONS: A linear association between PRS-SCZ and ECT outcome was uncovered. Although it is too early to adopt PRSs in ECT clinical decision making, these findings strengthen the positioning of PRS-SCZ as relevant to treatment response in psychiatry.

Shape and volume changes of the superior lateral ventricle after electroconvulsive therapy measured with ultra-high field MRI.

The subventricular zone (SVZ) of the lateral ventricles harbors neuronal stem cells in adult mammals. Rodent studies report neurogenic effects in the SVZ of electroconvulsive stimulation. We hypothesize that if this finding translates to depressed patients undergoing electroconvulsive therapy (ECT), this would be reflected in shape changes at the SVZ. Using T1-weighted MR images acquired at ultra-high field strength (7T), the shape and volume of the ventricles were compared from pre to post ECT after 10 ECT sessions (in patients twice weekly) or 5 weeks apart (controls) using linear mixed models with age and gender as covariates. Ventricle shape significantly changed and volume significantly decreased over time in patients for the left ventricle, but not in controls. The decrease in volume of the ventricles was associated to a decrease in depression scores, and an increase in the left dentate gyrus, However, the shape changes of the ventricles were not restricted to the neurogenic niche in the lateral walls of the ventricles, providing no clear evidence for neurogenesis as sole explanation of volume changes in the ventricles after ECT.

Genetic underpinnings of schizophrenia-related electroencephalographical intermediate phenotypes: A systematic review and meta-analysis.

Although substantial research into genetics of psychotic disorders has been conducted, a large proportion of their genetic architecture has remained unresolved. Electroencephalographical intermediate phenotypes (EIP) have the potential to constitute a valuable tool when studying genetic risk loci for schizophrenia, in particular P3b amplitude, P50 suppression, mismatch negativity (MMN) and resting state power spectra of the electroencephalogram (EEG). Here, we systematically reviewed studies investigating the association of single nucleotide polymorphisms (SNPs) with these EIPs and meta-analysed them when appropriate. We retrieved 45 studies (N = 34,971 study participants). Four SNPs investigated in more than one study were genome-wide significant for an association with schizophrenia and three were genome-wide suggestive, based on a lookup in the influential 2014 GWAS (Ripke et al., 2014). However, in our meta-analyses, rs1625579 failed to reach a statistically significant association with p3b amplitude decrease and rs4680 risk allele carrier status was not associated with p3b amplitude decrease or with impaired p50 suppression. In conclusion, evidence for SNP associations with EIPs remains limited to individual studies. Careful selection of EIPs and SNPs, combined with consistent reporting of effect sizes, directions of effect and p-values would aid future meta-analyses.