Pathological study of abnormal protein accumulation and its propagation in the brain of patients with dementia

2015 Fiscal Year Final Research Report

• Project/Area Number: 24500429
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: Tokyo Metropolitan Institute of Medical Science
• Principal Investigator: AKIYAMA Haruhiko 公益財団法人東京都医学総合研究所, 認知症・高次脳機能研究分野, 参事研究員 (20231839)
• Co-Investigator(Renkei-kenkyūsha): HASEGAWA Masato 公益財団法人東京都医学総合研究所, 認知症・高次脳機能研究分野, 分野長 (10251232) ; HOSOKAWA Masato 公益財団法人東京都医学総合研究所, 認知症・高次脳機能研究分野, 主席研究員 (00435116) ; ARAI Tetsuaki 筑波大学, 医学部精神科, 教授 (90291145)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 認知症 / 病理 / 異常蓄積蛋白 / 伝播

Outline of Final Research Achievements

The major cause of dementia is neurodegenerative diseases in which abnormally aggregated proteins form insoluble deposits in the brain. The distribution of these protein aggregates is consistent with the neuroanatomical architecture of the brain, a finding that suggests expansion of the lesions through the neural circuits. In Alzheimer’s disease, Abeta and tau are the principal proteins that are deposited in the brain. Tangle-predominant dementia (TPD) is characterized by heavy accumulation of tau in the limbic structures and virtual absence of Abeta. The nature of tau aggregates in TPD is similar to that in AD. We found that tau accumulation is much heavier in the nucleus accumbens in TPD than AD. In TPD, tau accumulation is heavier than AD in the hippocampal CA1 and the subiculum, the brain regions that give rise to significant projections to the nucleus accumbens. The finding supports a notion that the process of tau aggregation propagates through the neural circuits.

Free Research Field

脳神経科学（認知症の原因となる神経変性疾患の病理学）