LGI1 and early-onset autosomal dominant Alzheimer disease: One recent retrospective study of 13 patients (8 with follow-up scans) with comparison to patients with different forms of AE, Alzheimer’s disease, and healthy controls showed that patients with anti-LGI1 were found to have hypermetabolism in the medial temporal lobes, the pallidum, caudate, pons, olfactory, and inferior occipital gyri as well as hypometabolism in several frontoparietal regions [15].