Pre-emptive medicine for dementia ; when and how we inhibit amyloid deposition?

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  • Tomita Taisuke
    Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo

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  • 認知症への先制医療：アミロイド蓄積をいつ，どのように防ぐか
  • ニンチショウ エ ノ センセイ イリョウ : アミロイド チクセキ オ イツ,ドノ ヨウ ニ フセグ カ

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Abstract

Amyloid-βpeptide (Aβ) is the major component of senile plaques deposited in the brains of patients with Alzheimer disease (AD). Several lines of evidence suggest that the accumulation of A βis linked to the pathogenesis of AD. A βis derived from amyloid-βprecursor protein (APP) that is sequentially cleaved by two aspartate proteases, β- and γ- secretases. Advances in basic research and observational study implicate that that drugs that inhibit or modulate the proteolytic activity of these secretases could provide a disease- modifying therapy against AD as pre- emptive medicine. In addition, evolutional genome sequencing technologies reveal several genetic risk factors, which may impact on the onset of AD. In this review, I will discuss about recent status regarding the development of therapeutics for AD.

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