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An imbalance in KP metabolites may exacerbate hippocampal atrophy, cognitive decline, and depressive symptoms, highlighting a mechanistic link between KP dysregulation, excitotoxicity, and neuropsychiatric manifestations

Logistic regression models were used to calculate propensity scores, including as covariates: sex, onset, El Escorial category, use of riluzole, ALSFRS-R total score at baseline, FVC at baseline, time from diagnosis to the first available visit for not treated subjects or to the date of ALCAR treatment start for treated subjects, diagnostic delay (time from onset to diagnosis), age at baseline

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The partial rescue of the above-described symptomatology can be ascribed to the activity of other transporters such as ATB 0,+ (SLC6A14), MCT9, and probably, OCTN1 (SLC22A4) that accept carnitine with a much lower affinity if compared to OCTN2