第60回日本神経学会学術大会

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シンポジウム

[S-07] Extending the clinical spectrum of cerebral amyloid angiopathy (CAA)

2019年5月22日(水) 13:20 〜 14:50 第10会場 (大阪国際会議場12F グラントック)

座長：Steven M. Greenberg（Massachusetts General Hospital, USA／Harvard Medical School, USA）, 山田 正仁（金沢大学大学院医薬保健学総合研究科脳老化・神経病態学(神経内科学））

Cerebral amyloid angiopathy (CAA) , a common finding in the aging brain, is caused by accumulation of amyloid beta protein in the cerebral vasculature. Recent studies have revealed that CAA has a wider clinical spectrum than previously recognized. CAA should be in differential diagnosis of patients with lobar intracerebral hemorrhage, cognitive impairment, transient neurological symptoms, headache, and other neurological manifestations. Understanding of the growing clinical spectrum of CAA would lead to a more appropriate approach towards management of patients with CAA-related neurological disorders. In this symposium, experts in this field discuss (1) the wide clinical spectrum of CAA-related cerebrovascular disorders, (2) CAA-related cognitive impairment and inflammation, and (3) management of CAA, including current clinical implications and future perspectives for therapies against CAA.

[S-07-1] 脳アミロイドアンギオパチー関連脳血管障害の臨床スペクトル

薬師寺 祐介, 原 英夫 (佐賀大学医学部　内科学講座 神経内科)

Cerebral amyloid angiopathy (CAA) , a common finding in the aging brain, is caused by accumulation of amyloid beta protein in the cerebral vasculature. Recent studies have revealed that CAA has a wider clinical spectrum than previously recognized. CAA should be in differential diagnosis of patients with lobar intracerebral hemorrhage, cognitive impairment, transient neurological symptoms, headache, and other neurological manifestations. Understanding of the growing clinical spectrum of CAA would lead to a more appropriate approach towards management of patients with CAA-related neurological disorders. In this symposium, experts in this field discuss (1) the wide clinical spectrum of CAA-related cerebrovascular disorders, (2) CAA-related cognitive impairment and inflammation, and (3) management of CAA, including current clinical implications and future perspectives for therapies against CAA.

[S-07-2] 脳アミロイドアンギオパチー関連炎症および認知機能障害

坂井 健二, 山田 正仁 (金沢大学大学院　脳老化・神経病態学（神経内科学）)

Cerebral amyloid angiopathy (CAA) , a common finding in the aging brain, is caused by accumulation of amyloid beta protein in the cerebral vasculature. Recent studies have revealed that CAA has a wider clinical spectrum than previously recognized. CAA should be in differential diagnosis of patients with lobar intracerebral hemorrhage, cognitive impairment, transient neurological symptoms, headache, and other neurological manifestations. Understanding of the growing clinical spectrum of CAA would lead to a more appropriate approach towards management of patients with CAA-related neurological disorders. In this symposium, experts in this field discuss (1) the wide clinical spectrum of CAA-related cerebrovascular disorders, (2) CAA-related cognitive impairment and inflammation, and (3) management of CAA, including current clinical implications and future perspectives for therapies against CAA.

[S-07-3] Extending the clinical spectrum of cerebral amyloid angiopathy (CAA)

Steven M. Greenberg1,2 (1.Massachusetts General Hospital, 2.Harvard Medical School)

Cerebral amyloid angiopathy (CAA) , a common finding in the aging brain, is caused by accumulation of amyloid beta protein in the cerebral vasculature. Recent studies have revealed that CAA has a wider clinical spectrum than previously recognized. CAA should be in differential diagnosis of patients with lobar intracerebral hemorrhage, cognitive impairment, transient neurological symptoms, headache, and other neurological manifestations. Understanding of the growing clinical spectrum of CAA would lead to a more appropriate approach towards management of patients with CAA-related neurological disorders. In this symposium, experts in this field discuss (1) the wide clinical spectrum of CAA-related cerebrovascular disorders, (2) CAA-related cognitive impairment and inflammation, and (3) management of CAA, including current clinical implications and future perspectives for therapies against CAA.