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With the aim of identifying associations between cognitive impairment including memory impairment and \u03b1-synuclein pathology, 148 consecutive patients with pathologically proven multiple system atrophy were reviewed. Among them, 118 (79.7%) were reported to have had normal cognition in life, whereas the remaining 30 (20.3%) developed cognitive impairment. Twelve of them had pure frontal-subcortical dysfunction, defined as the presence of executive dysfunction, impaired processing speed, personality change, disinhibition or stereotypy; six had pure memory impairment; and 12 had both types of impairment. Semi-quantitative analysis of neuronal cytoplasmic inclusions in the hippocampus and parahippocampus revealed a disease duration-related increase in neuronal cytoplasmic inclusions in the dentate gyrus and cornu ammonis regions 1 and 2 of patients with normal cognition. In contrast, such a correlation with disease duration was not found in patients with cognitive impairment. Compared to the patients with normal cognition, patients with memory impairment (pure memory impairment: n\u2009=\u20096; memory impairment + frontal-subcortical dysfunction: n\u2009=\u200912) had more neuronal cytoplasmic inclusions in the dentate gyrus, cornu ammonis regions 1\u20134 and entorhinal cortex. In the multiple system atrophy mixed pathological subgroup, which equally affects the striatonigral and olivopontocerebellar systems, patients with the same combination of memory impairment developed more neuronal inclusions in the dentate gyrus, cornu ammonis regions 1, 2 and 4, and the subiculum compared to patients with normal cognition. Using patients with normal cognition (n\u2009=\u200918), frontal-subcortical dysfunction (n\u2009=\u200912) and memory impairment + frontal-subcortical dysfunction (n\u2009=\u200918), we further investigated whether neuronal or glial cytoplasmic inclusions in the prefrontal, temporal and cingulate cortices or the underlying white matter might affect cognitive impairment in patients with multiple system atrophy. We also examined topographic correlates of frontal-subcortical dysfunction with other clinical symptoms. Although no differences in neuronal or glial cytoplasmic inclusions were identified between the groups in the regions examined, frontal release signs were found more commonly when patients developed frontal-subcortical dysfunction, indicating the involvement of the frontal\u2013subcortical circuit in the pathogenesis of frontal-subcortical dysfunction. Here, investigating cognitive impairment in the largest number of pathologically proven multiple system atrophy cases described to date, we provide evidence that neuronal cytoplasmic inclusion burden in the hippocampus and parahippocampus is associated with the occurrence of memory impairment in multiple system atrophy. Further investigation is necessary to identify the underlying pathological basis of frontal-subcortical dysfunction in multiple system atrophy.<\/jats:p>","DOI":"10.1093\/brain\/awaa126","type":"journal-article","created":{"date-parts":[[2020,4,5]],"date-time":"2020-04-05T11:07:28Z","timestamp":1586084848000},"page":"1798-1810","source":"Crossref","is-referenced-by-count":46,"title":["Hippocampal \u03b1-synuclein pathology correlates with memory impairment in multiple system atrophy"],"prefix":"10.1093","volume":"143","author":[{"given":"Yasuo","family":"Miki","sequence":"first","affiliation":[{"name":"Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"},{"name":"Department of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandrine 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UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eiki","family":"Tsushima","sequence":"first","affiliation":[{"name":"Department of Comprehensive Rehabilitation Science, Hirosaki University Graduate School of Health Sciences, Hirosaki 036-8564, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zane","family":"Jaunmuktane","sequence":"first","affiliation":[{"name":"Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew J","family":"Lees","sequence":"first","affiliation":[{"name":"Reta Lila Weston Institute of Neurological Studies, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas T","family":"Warner","sequence":"first","affiliation":[{"name":"Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"},{"name":"Reta Lila Weston Institute of Neurological Studies, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Niall","family":"Quinn","sequence":"first","affiliation":[{"name":"UCL Queen Square Institute of Neurology, London WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helen","family":"Ling","sequence":"first","affiliation":[{"name":"Queen Square Brain Bank for Neurological Disorders, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"},{"name":"Reta Lila Weston Institute of Neurological Studies, UCL Queen Square Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janice L","family":"Holton","sequence":"first","affiliation":[{"name":"Queen Square Brain Bank for Neurological 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