Cerebellar ataxia is a heterogeneous group of neural disorders clinically characterized by cerebellar dysfunction. The diagnosis of patients with progressive cerebellar ataxia is complex due to the direct correlation with other neuron diseases. Although there is still no cure for this pathological condition, some metabolic, hereditary, inflammatory, and immunological factors affecting cerebellar ataxia are being studied and which may become therapeutic targets. Advances in studying the neuroanatomy, pathophysiology, and molecular biology of the cerebellum contributes to better understand the mechanisms behind the development of this disorder. In this study, we analyzed the neuromodulatory role of the AMP-activated protein kinase (AMPK) on cerebellar ataxia induced by the neurotoxin 3-acetylpyridine (3-AP) in brain stem and cerebellum, after pre-treatment with metformin, a pharmacological indirect activator of AMPK. The results shown here suggest that AMPK activation in the brain stem and cerebellum leads to a significant reduction in neuroinflammation in these regions. AMPK was able to restore the changes in fatty acid composition and pro-inflammatory cytokines caused by 3-AP, suggesting that the action of AMPK seems to result in a possible neuroprotection on the cerebellar ataxia model.