The intersection of amyloid β and tau in glutamatergic synaptic dysfunction and collapse in Alzheimer's disease.
The intersection of amyloid β and tau in glutamatergic synaptic dysfunction and collapse in Alzheimer's disease.
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DOI：
10.1016/j.arr.2013.03.002
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发表时间：
2013-06
影响因子：
13.1
通讯作者：
Spires-Jones, Tara L.
中科院分区：
文献类型：
--
作者：
Crimins, Johanna L.;Pooler, Amy;Polydoro, Manuela;Luebke, Jennifer I.;Spires-Jones, Tara L.
在发育过程中形成的神经元之间的突触连接保持可塑性，并能够在整个生命周期中适应，从而实现学习和记忆。然而，在衰老过程中，特别是在神经退行性疾病中，突触变得功能障碍和退化，导致痴呆。在阿尔茨海默氏病（AD）的情况下，突触丧失是认知下降的最强病理相关性，表明突触变性在痴呆中起核心作用。在过去的十年中，已经出现了强有力的证据表明，寡聚形式的淀粉样蛋白β，在AD大脑中的老年斑中积累的蛋白质，有助于突触结构和功能的退化。最近的数据表明，病理形式的tau蛋白，其在AD脑中的神经元缠结中积累，也引起突触功能障碍和丧失。在这篇综述中，我们将提出的情况下，可溶性形式的淀粉样蛋白β和tau蛋白作用于突触，导致神经网络功能障碍，并进一步认为这两种病理蛋白可能会共同作用，导致突触病理。这些数据可能对靶向神经退行性疾病中的可溶性病理蛋白以预防或逆转认知能力下降具有广泛的意义。
The synaptic connections that form between neurons during development remain plastic and able to adapt throughout the lifespan, enabling learning and memory. However, during aging and in particular in neurodegenerative diseases, synapses become dysfunctional and degenerate, contributing to dementia. In the case of Alzheimer’s disease (AD), synapse loss is the strongest pathological correlate of cognitive decline, indicating that synaptic degeneration plays a central role in dementia. Over the past decade, strong evidence has emerged that oligomeric forms of amyloid beta, the protein that accumulates in senile plaques in the AD brain, contribute to degeneration of synaptic structure and function. More recent data indicate that pathological forms of tau protein, which accumulate in neurofibrillary tangles in the AD brain, also cause synaptic dysfunction and loss. In this review, we will present the case that soluble forms of both amyloid beta and tau protein act at the synapse to cause neural network dysfunction, and further that these two pathological proteins may act in concert to cause synaptic pathology. These data may have wide-ranging implications for the targeting of soluble pathological proteins in neurodegenerative diseases to prevent or reverse cognitive decline.
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影响因子：
16.2
作者：
Hoover, Brian R.;Reed, Miranda N.;Su, Jianjun;Penrod, Rachel D.;Kotilinek, Linda A.;Grant, Marianne K.;Pitstick, Rose;Carlson, George A.;Lanier, Lorene M.;Yuan, Li-Lian;Ashe, Karen H.;Liao, Dezhi
通讯作者：
Liao, Dezhi
DOI：
10.1016/s0006-291x(84)80190-4
发表时间：
1984-01-01
影响因子：
3.1
作者：
GLENNER, GG;WONG, CW
通讯作者：
WONG, CW
影响因子：
16.2
作者：
Ishihara, T;Hong, M;Lee, VMY
通讯作者：
Lee, VMY
DOI：
10.1073/pnas.94.1.298
发表时间：
1997-01-07
影响因子：
11.1
作者：
Alonso, AD;GrundkeIqbal, I;Iqbal, K
通讯作者：
Iqbal, K
影响因子：
25
作者：
Cleary, JP;Walsh, DM;Ashe, KH
通讯作者：
Ashe, KH