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Retinoids are involved in adult brain function and in neurodegenerative diseases. Decreased expression of synaptic
plasticity markers and metabolic changes induced by 14 weeks of vitamin A deprivation (VAD14) were previously
evidenced in rat brain. We evaluate early metabolic changes (by HRMAS proton NMR spectroscopy) on biopsies of cortex,
hippocampus and striatum (i) during VAD and (ii) after all trans Retinoic Acid administration.
In 10 wk VAD (VAD10), metabolic changes appeared in the cortex: (i) N-acetyl aspartate (NAA, +15%, P=0.05 vs C10), a
neuronal density indicator, (ii) glutathione (GSH, +30%, P=0.05 vs C10), an antioxidant status marker. Concerning the impact
of VAD duration, the NAA/GSH ratio in cortex, hippocampus and striatum was unchanged in all controls, whereas it
decreased in striatum and hippocampus of VAD10 and in striatum and cortex of VAD14. ATRA had an apparent regulatory
action by increasing NAA/GSH ratio in hippocampus (VAD10+ATRA vs VAD10: +34%, P=0.03), the striatal ratio being rescued
to control level. Gene expression of BACE and APP, which are amyloidogenesis markers, were unchanged in
VAD10 whereas VAD14 seemed to activate cortical amyloidogenesis.
Hypoexpression of retinoid signaling during a short 10 wk period has consequences on brain metabolic profile and precedes
the impaired expression of both amyloidogenesis and synaptic plasticity markers. Rat nutritional VAD represents a
model of accelerated aging which mimics the course of aging. The NAA/GSH ratio reflects the balance between neuronal
health and protection against reactive oxygen species, and could thus serve as a marker of brain health.