Amyloid Beta: Multiple Mechanisms of Toxicity and Only Some Protective Effects?

被引:143
作者
Carrillo-Mora, Paul [1 ]
Luna, Rogelio [2 ]
Colin-Barenque, Laura [3 ]
机构
[1] Inst Nacl Rehabil, Serv Rehabil Neurol, Dept Neurorrehabil, Mexico City 14389, DF, Mexico
[2] Univ Nacl Autonoma Mexico, Inst Fisiol Celular Neurociencas, Dept Neurociencia Cognit, Mexico City 04510, DF, Mexico
[3] Univ Nacl Autonoma Mexico, FES Iztacala, Dept Neurociencias, Tlalnepantla 54090, Mex, Mexico
关键词
LONG-TERM POTENTIATION; NICOTINIC ACETYLCHOLINE-RECEPTORS; ACTIVATED PROTEIN-KINASE; ALZHEIMERS-DISEASE; A-BETA; PRECURSOR PROTEIN; OXIDATIVE STRESS; SYNAPTIC PLASTICITY; PLAQUE CORE; MITOCHONDRIAL DYSFUNCTION;
D O I
10.1155/2014/795375
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Amyloid beta (A beta) is a peptide of 39-43 amino acids found in large amounts and forming deposits in the brain tissue of patients with Alzheimer's disease (AD). For this reason, it has been implicated in the pathophysiology of damage observed in this type of dementia. However, the role of A beta. in the pathophysiology of AD is not yet precisely understood. A beta has been experimentally shown to have a wide range of toxic mechanisms in vivo and in vitro, such as excitotoxicity, mitochondrial alterations, synaptic dysfunction, altered calcium homeostasis, oxidative stress, and so forth. In contrast, A beta has also shown some interesting neuroprotective and physiological properties under certain experimental conditions, suggesting that both physiological and pathological roles of A beta may depend on several factors. In this paper, we reviewed both toxic and protective mechanisms of A beta to further explore what their potential roles could be in the pathophysiology of AD. The complete understanding of such apparently opposed effects will also be an important guide for the therapeutic efforts coming in the future.
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页数:15
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