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一种降血压药可治疗老年健忘

随着年纪变大,我们的记性开始变差,经常忘了车钥匙放哪里,或者想不起那个经常见面的人的名字。现在一项新研究找到了这种所谓工作记忆“认知缺失”的原因,并认为这种情况可以逆转。

美国耶鲁大学科研人员发现,相比年轻人,中老年人大脑的神经网络连接更为脆弱,活动也不那么频繁。正如他们在《自然》周刊上所指出的那样,对动物的实验证明,可以用当前治疗高血压的一种药物来扭转这种认知缺失

随着年纪变大,人变得越来越容易忘事或者难以集中注意力,一些认知功能也难以完成。虽然很长时间以来大家都认为这种缺失与年龄有关,但至今还不知道造成这种认知缺失的生物学原因。

耶鲁大学神经科学研究人员对处于青年、中年和老年三个不同年龄段的猴子进行研究,分析它们前额叶皮层(大脑负责认知功能和解决问题的区域)神经细胞的活动如何随着衰老而变化。

这些猴子被要求进行一些需要使用工作记忆的活动,例如回想目标物放置地、组织表演或同时进行多项活动等。研究人员发现,青年猴子前额叶皮层的神经连接能够在实验活动中保持高频率的“放电”,而年老猴子神经细胞放电程度更弱且时间更短

然而当科研人员使用一种化学成分封锁神经信号重复这些实验时,却使这种神经细胞损坏得到修复,年老猴子达到与青年猴子相似的活动水平。

科研人员认为,衰老会导致一种被称为cAM P的分子过度积累,它可能导致神经信号变弱。使用某些化学成分封锁或者禁止这类分子的活动就可以逆转神经细胞的信号连接方式,改善它们的功能。

因年纪变大而产生的认知缺失会给生活带来严重影响,妨碍我们工作或独立生活能力。研究人员认为,现有药物能够改善神经联系功能,其中一种用于治疗高血压的药物能够禁止cAM P分子的活动,修复工作记忆,但任何药物都有待进一步的临床验证方可使用。

英文论文摘要:

Nature (2011) doi:10.1038/nature10243

Neuronal basis of age-related working memory decline

Abstract:

Many of the cognitive deficits of normal ageing (forgetfulness, distractibility, inflexibility and impaired executive functions) involve prefrontal cortex (PFC) dysfunction. The PFC guides behaviour and thought using working memory, which are essential functions in the information age. Many PFC neurons hold information in working memory through excitatory networks that can maintain persistent neuronal firing in the absence of external stimulation. This fragile process is highly dependent on the neurochemical environment. For example, elevated cyclic-AMP signalling reduces persistent firing by opening HCN and KCNQ potassium channels. It is not known if molecular changes associated with normal ageing alter the physiological properties of PFC neurons during working memory, as there have been no in vivo recordings, to our knowledge, from PFC neurons of aged monkeys. Here we characterize the first recordings of this kind, revealing a marked loss of PFC persistent firing with advancing age that can be rescued by restoring an optimal neurochemical environment. Recordings showed an age-related decline in the firing rate of DELAY neurons, whereas the firing of CUE neurons remained unchanged with age. The memory-related firing of aged DELAY neurons was partially restored to more youthful levels by inhibiting cAMP signalling, or by blocking HCN or KCNQ channels. These findings reveal the cellular basis of age-related cognitive decline in dorsolateral PFC, and demonstrate that physiological integrity can be rescued by addressing the molecular needs of PFC circuits.

Figure 1: Age-related changes in the PFC networks that subserve working memory.

Figure 1: Age-related changes in the PFC networks that subserve working memory.

Figure 2: Age-dependent decline in the spatially tuned, persistent firing of dorsolateral PFC DELAY neurons.

Figure 2: Age-dependent decline in the spatially tuned, persistent firing of dorsolateral PFC DELAY neurons.

Figure 3: Firing rates of dorsolateral PFC CUE cells remain stable in aged monkeys.

Figure 3: Firing rates of dorsolateral PFC CUE cells remain stable in aged monkeys.

 

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摘要
一项新研究找到了这种所谓工作记忆“认知缺失”的原因,并认为这种情况可以逆转。
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