Background and objectives: Movement disorders are an underrecognized phenomenon in Myelin Oligodendrocyte Glycoprotein-Associated Disease (MOGAD). The aim of this paper was to summarize all movement disorders previously described in MOGAD. Materials and Methods: We conducted a systematic literature search in PubMed, Web of Science, and Scopus in English, focusing on patients with MOGAD exhibiting a movement disorder, i.e., ataxia, tremor, dystonia, parkinsonism, chorea, athetosis, myoclonus, ballism, tics, stereotypies, dyskinesia. Results: We included 58 studies, with a total of 91 patients with MOGAD and a movement disorder (45.6% male, 54.4% female). Movement disorders had a mean latency of 2.1 years (±6.9, 0–42) after MOGAD onset; however, they could be the presenting feature (in approximately 70% of cases), especially in pediatric patients. Cerebellar ataxia was the most common movement disorder, occurring in 77 patients (84.6%). Tremor, postural and/or kinetic, was the second most common movement disorder (15%). Dystonia was reported in 8.8%, presenting as cervical, or limb dystonia or stereotyped dystonic episodes. Myoclonus and hypokinetic movement disorders were rare. Subcortical (in 60%), brainstem and cerebellar lesions (in 50% respectively) were the most common imaging findings. The most common accompanying symptoms were encephalopathy, fever and headache. Approximately half of the patients made a full recovery, and the other half showed a significant improvement in the movement disorder after immunomodulatory treatment, most commonly steroids. Conclusions: The new onset of a movement disorder, especially ataxia, in a young patient should prompt the search for MOGAD or can indicate a relapse in patients with an established diagnosis.

Background: Over the last decade, numerous studies have investigated the administration of monoclonal anti-amyloid antibodies (AAAs) as a therapeutic approach in Alzheimer’s disease (AD). The purpose of this umbrella review is to summarize current knowledge concerning the efficacy and safety of FDA- and EMA-approved AAAs for AD, namely, lecanemab and donanemab. Methods: We conducted a literature search in the PubMed, Scopus, and Web of Science databases in English, focusing on systematic reviews and/or meta-analyses, assessed by AMSTAR 2, concerning clinical and imaging efficacy, i.e., cognitive improvement and reduction of beta-amyloid on PET scan, as well as safety, i.e., adverse events and amyloid-related imaging abnormalities (ARIA). The extracted review-level dataset was entered into SPSS Version 26 for descriptive statistical analysis. Results: This umbrella review included 11 systematic reviews and/or meta-analyses. Patients treated with lecanemab or donanemab showed statistically significant changes on cognitive scales such as the Clinical Dementia Rating-Sum of Boxes (CDR-SB) (mean effect estimate −0.485, SD = 0.152, −0.70 to −0.34) and the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), but most were below or around clinically meaningful thresholds. Lecanemab and donanemab showed a statistically significant decrease in amyloid PET outcomes, including centiloids or the standardized uptake value ratio. Both antibodies were linked to ARIA, including amyloid-related imaging abnormalities-edema (ARIA-E OR 8.32–12.26) and amyloid-related imaging abnormalities-hemorrhage (ARIA-H OR 2–5.77), especially in ApoEε4 carriers. Conclusions: Lecanemab and donanemab are biologically active drugs for the treatment of early AD, with cognitive benefits below or around the clinically meaningful threshold. They are, however, associated with increased ARIA risk. Their administration depends upon careful patient selection, shared decision-making, and clear communication regarding expectations.