This study investigates the effects of a ketogenic diet (KD) on the brain proteome in Genetic Absence Epilepsy Rats from Strasbourg (GAERS), a model of genetic absence epilepsy. The ketogenic diet is a therapeutic intervention for epilepsy, yet its mechanisms remain incompletely understood. Thirty-day-old male GAERS rats were fed a KD (88.8% fat, 10.2% protein, 1% carbohydrate; n = 4) or a normal diet (ND; n = 3), with Wistar rats (n = 3) as healthy controls. A shotgun proteomics approach with data-dependent acquisition was used to analyze the somatosensory cortex (SCx) and hippocampus (Hipp). Data were processed with MaxQuant and Perseus. Compared to Wistars, GAERS-ND rats showed significant alterations in 526 proteins in SCx and 612 in Hipp. KD treatment significantly altered 122 proteins in SCx and 124 in Hipp of GAERS. Notably, KD reversed the expression of 22 proteins in SCx and 32 in Hipp to levels observed in controls. Most KD-affected proteins were synaptic (72% SCx, 76.6% Hipp) and mitochondrial. Pathway analysis indicated KD regulates axon guidance, neurodevelopment, and metabolism in SCx, and autophagy, mitophagy, and Rho GTPase signaling in Hipp. The workflow of the experimental design is provided in Fig. 1.

Purpose: This study investigated the effects of ketogenic diet (KD) intervention on the cortical proteome in genetic absence epilepsy rats from Strasbourg (GAERS), a well‐established model of absence epilepsy. The ketogenic diet is a therapeutic intervention for epilepsy, yet its mechanisms remain incompletely understood. Method: Thirty‐day‐old male GAERS rats were fed a KD (88.8% fat, 10.2% protein, 1% carbohydrate; n = 4) or a normal diet (ND; n = 3), with Wistar rats ( n = 3) as healthy controls. A shotgun proteomics approach with data‐dependent acquisition (DDA) was used to analyze the somatosensory cortex (SCx), a key cortical driver of absence seizures. Data were processed with MaxQuant and Perseus. Findings: Compared to Wistars, GAERS‐ND rats showed significant alterations in 526 proteins in SCx and KD treatment significantly altered 121 proteins in SCx of GAERS. Notably, KD was associated with partial shifts in the expression patterns of 22 proteins toward those observed in Wistar controls. Most KD‐affected proteins were synaptic (72% SCx) and mitochondrial. Pathway analysis indicated that ketogenic diet–associated protein changes were enriched in axon guidance, neurodevelopment, and metabolic pathways in the somatosensory cortex. Conclusion: Together, these results suggest that synaptic and mitochondrial protein alterations in this region are associated with cortical molecular adaptations observed under ketogenic diet administration in absence epilepsy.

Downy mildew pathogens are obligate biotrophic oomycetes responsible for destructive diseases in many agricultural crops. Among them, Plasmopara halstedii, the causal agent of sunflower downy mildew, represents a major threat to sunflower production worldwide. While extensive research has focused on the genetics of host resistance and the pathogenic variability of this organism, information regarding the proteins involved in its infection process remains limited. Proteomic approaches have increasingly been used to study plant–pathogen interactions, as they enable the direct identification of proteins produced during infection. In oomycete pathogens such as Phytophthora species, proteomic studies have revealed numerous proteins associated with host colonization, virulence, and stress adaptation. However, comparable large-scale proteomic investigations are still scarce for downy mildew pathogens, particularly for P. halstedii. This review summarizes current knowledge on proteomic studies in oomycete plant pathogens and discusses the limited information available on proteins of P. halstedii. The review also highlights key research gaps and potential directions for future proteomic investigations.