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Alzheimer's Disease, Other Dementia, Aging

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Age dependent change of the distribution of amyloid beta protein in macaque monkeys

  • P3-278
  • 木村 活生 / Katsuo Kimura:1,2 井上 謙一 / Ken-ichi Inoue:1 田中 章景 / Fumiaki Tanaka:2 高田 昌彦 / Masahiko Takada:1 
  • 1:京都大 霊長研 統合脳 / Sys Neurosci, Pri Res Inst, Kyoto Univ, Inuyama, Japan 2:横浜市大 神経内科 / Dept Neurol, Yokohama City Univ, Yokohama, Japan 

Alzheimer's disease (AD) is the most common form of dementia, accounting for approximately 60% of all dementia cases. AD is characterized by gradual deterioration of cognitive functions, including memory, and neuropsychiatric symptoms. Extracellular amyloid plaques composed primarily of aggregated amyloid-beta protein (a-beta) are one of the main pathological features in the AD brain, and are distributed predominantly in the temporal cortex, amygdala, and hippocampus. When the a-beta deposition begins and how it proceeds and spreads remain unclear. In the present study, we investigated the age-dependent changes of a-beta distribution in macaque brains. Fourteen macaque monkeys (seven Japanese monkeys, six cynomolgus monkeys, and one rhesus monkey) ranging 10-31 years old were used. In these monkeys, counts of immunohistochemically stained a-beta plaques were performed. No a-beta depositions were found in the brains at younger ages than 21 years. As the age went, the number of a-beta plaques was gradually increased. These depositions first emerged in the amygdala and nucleus accumbens and then spread to the temporal cortical areas, cingulate gyrus, and hippocampus. In the brains at older ages than 26 years, a-beta depositions further appeared in the orbitofrontal cortex and striatum. The number of a-beta plaques in the far-aged brains (at older ages than 26 years) was six-to-seven times as many as in the younger brains. However, no marked cognitive deficits were apparently observed even in the far-aged monkeys. The present results indicate that the distribution and progression of a-beta plaques in aged macaque brains display a similar pattern to those seen in healthy aged humans as well as in AD patients. Therefore, the aged macaque monkeys might represent a potential presymptomatic model for AD.

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