Long-term lithium treatment reduces glucose metabolism in the cerebellum and hippocampus of nondemented older adults: an [¹⁸F]FDG-PET study.

摘要: Lithium modulates several intracellular pathways related to neuroplasticity and resilience against neuronal injury. These properties have been consistently reported in experimental models, involve the up-regulation of neurotrophic response autophagy, down-regulation apoptosis, oxidative stress, inflammation. Clinical epidemiological studies bipolar disorder show that acute treatment with lithium increases plasma concentrations brain-derived factor, long-term lowers risk dementia. Neuroimaging indicate use is further associated increased cortical thickness larger hippocampal volumes. The objective present study was evaluate whether these neurobiological reflect regional brain glucose metabolism, as shown by [(18)F]FDG-PET. Participants (n = 19) were nondemented older adults recruited at end point a controlled trial addressing clinical biological effects sample patients amnestic mild cognitive impairment. Twelve who had received low-dose carbonate for 4 years compared seven matched controls. Chronic not any significant increase metabolism studied areas. Conversely, we found reduction uptake clusters cerebellum both hippocampi. findings evidence toxicity. implications need be clarified future studies, particularly light potential disease-modifying approach certain neurodegenerative disorders, namely, Alzheimer's disease amyotrophic lateral sclerosis.