【摘 要】
：
Transthyretin (TTR) is a protective molecule in Atzheimers Disease (AD), binds A-Beta peptide inhibiting its aggregation and toxicity.TTR is early decreased in the cerebrospinal fluid and sera of AD p
【机 构】
：
Instituto de Biologia Molecular e Celular-IBMC Portugal
【出 处】
：
2013百奥泰波兰重大疾病临床峰会
论文部分内容阅读
Transthyretin (TTR) is a protective molecule in Atzheimers Disease (AD), binds A-Beta peptide inhibiting its aggregation and toxicity.TTR is early decreased in the cerebrospinal fluid and sera of AD patients, and we showed that this decrease is observed early in disease development as indicated by the lower sera TTR levels measured in patients with mild cognitive impairment (MCI)and with AD; we also reported that TTR levels correlate with disease state.We also showed that sera TTR from MCI and AD patients binds less T4 than TTR from controls indicating TTR is destabilized and its clearance accelerated, explaining the lower levels found.We suggested TTR stability as a key factor in TTR/A-Beta interaction upon the observation that different TTR mutations bind differently to A-Beta, correlating inversely with TTR amyloidogenic potential; we hypothesized the use of small compounds known to stabilize the TTR tetrameric fold for improving TTR binding to A-Beta, and we already identified drugs with such ability.
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