Epigenetic modulation of cognitive function: toward new treatment models

Background The current translational work is an outgrowth of a mechanistic framework in rodents with cognitive deficits and depressive-like traits, wherein the levels pivotal mitochondrial metabolite acetyl-L-carnitine (LAC) are decreased signal to brain abnormal activity histone acetyltransferase expression genes key for neuronal plasticity, such as mGlu2 (a inhibitor glutamate release). Yet, role this emerging signaling pathway plasticity remains be fully determined subjects impairments (CI). Method Here we performed ultraperformance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS) measure peripheral LAC related free-carnitine cohort (CI, n = 29) age- sex-matched cognitively healthy controls (HC, 32). Next, multiple regression analysis investigate relationship between metabolism clinical characteristics. Result Decreased CI compared HC (p 0.02), potential sex differences 0.03). Incorporation these new measures into canonical biomarker model improved diagnostic accuracy Conclusion Our findings suggest that deficiency LAC, levels, might define phenotypes CI. Ongoing studies ascertaining its main free-carnitine, relation specific domains.