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Les m\u00e9canismes mis en \u0153uvre dans la physiopathologie de la MA sont de mieux en mieux connus, et incluent l\u2019accumulation de plaques amylo\u00efdes et de d\u00e9g\u00e9n\u00e9rescences neurofibrillaires. L\u2019augmentation de l\u2019inflammation et du stress oxydant et l\u2019alt\u00e9ration du m\u00e9tabolisme c\u00e9r\u00e9bral du glucose aggravent la pathologie en r\u00e9duisant l\u2019activit\u00e9 neuronale en perturbant la fonction mitochondriale. \u00c0 l\u2019heure actuelle, le traitement de cette pathologie regroupe diff\u00e9rentes approches bien que ces interventions n\u2019aient pas un effet curatif, mais uniquement compensatoire. L\u2019alimentation c\u00e9tog\u00e8ne, pauvre en glucides et enrichie en lipides, coupl\u00e9e \u00e0 une prise de triglyc\u00e9rides \u00e0 cha\u00eene moyenne (MCT), favorise la production de corps c\u00e9toniques, substrats \u00e9nerg\u00e9tiques qui pourraient pr\u00e9senter des effets neuroprotecteurs b\u00e9n\u00e9fiques pour les personnes atteintes de la MA. Une telle prise en charge nutritionnelle pourrait limiter la progression de la maladie et am\u00e9liorer les capacit\u00e9s cognitives des patients. 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