An explorers of Alzheimer's disease——Professor Zhang Chen

doi:10.3969/j.issn.1006-7795.2020.05.007

Abstract

Abstract: Dr. Zhang Chen, Professor and Dean, School of Basic Medical Sciences, Capital Medical University. As the most common neurodegenerative disease, the early causes of Alzheimer's disease (AD) remain unclear. Dr. Zhang has long been devoted himself to exploring the early neurological pathogenesis of AD. He found that short-term plasticity abnormality is an early pathological event in AD cases, and this deficit is caused by intracellular ryanodine receptor deficiency. Furthermore, using the two-photon method to study neural circuit activities on awake animals, he found that the prefrontal cortex incapable of encoding short-term memory is an earlier pathological event of AD compared with short-term plasticity deficits. Moreover, Dr. Zhang has identified several novel candidates (PTPRO, ABHD6 and others) functioning in the process of synapse formation and synaptic transmission, providing potential candidates for AD treatments.

Key words: Alzheimer's disease, synaptic dysfunction, new synaptic regulatory molecules

CLC Number:

R742

Zhang Chen. An explorers of Alzheimer's disease——Professor Zhang Chen[J]. Journal of Capital Medical University, 2020, 41(5): 756-762.

0
/ / Recommend

Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks

URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2020.05.007

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2020/V41/I5/756

References

[1] Lu B, Nagappan G, Guan X, et al. BDNF-based synaptic repair as a disease-modifying strategy for neurodegenerative diseases[J]. Nat Rev Neurosci, 2013,14(6):401-416.
[2] Selkoe D J. Alzheimer's disease is a synaptic failure[J]. Science, 2002,298(5594):789-791.
[3] Pascale N L, Maria C B, Lei C, et al. Synaptic targeting by Alzheimer's-related amyloid oligomers[J]. J Neurosci, 2004,24(45):10191-10200.
[4] De Felice F G, Decker H, Klein W L, et al. Protection of synapses against Alzheimer's-linked toxins:insulin signaling prevents the pathogenic binding of Aβ oligomers[J]. Proc Natl Acad Sci,2009,106(6):1971-1976.
[5] Mielke M L, Spires-Jones T L, Hashimoto T, et al. Oligomeric amyloid associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques[J]. Proc Natl Acad Sci,2009,106(10):4012-4017.
[6] Palop J J, Mucke L. Amyloid-Β-induced neuronal dysfunction in Alzheimer's disease:From synapses toward neural networks[J]. Nat Neurosci,2010,13(7):812-818.
[7] Zhang D, Zhang C, Ho A, et al. Inactivation of presenilins causes pre-synaptic impairment prior to post-synaptic dysfunction[J]. J Neurochem,2010,115(5):1215-1221.
[8] Zhang C, Wu B, Beglopoulos V, et al. Presenilins are essential for regulating neurotransmitter release[J]. Nature,2009,460(7255):632-636.
[9] Tian Y, Yang C, Cui Y, et al. An excitatory neural assembly encodes short-term memory in the prefrontal cortex[J]. Cell Rep,2018,22(7):1734-1744.
[10] Wang Y, Su F, Wang S, et al. Efficient implementation of convolutional neural networks in the data processing of two-photon in vivo imaging[J]. Bioinformatics,2019,35(17):1-3.
[11] Zhang L, Wei M, Shao L, et al. Enhanced parylene-C fluorescence as a visual marker for neuronal electrophysiology applications[J]. Lab Chip,2018,18(23):3539-3549.
[12] Su F, Yuan P, Wang Y, et al. The superior fault tolerance of artificial neural network training with a fault/noise injection-based genetic algorithm[J]. Protein Cell,2016, 7(10):735-748.
[13] Shang S, Wang C, Guo C, et al. The formation and extinction of fear memory in tree shrews[J]. Front Behav Neurosci,2015,9:204.
[14] Jiang W, Hua R, Wei M, et al. An optimized method for high-titer lentivirus preparations without ultracentrifugation[J]. Sci Rep,2015,5:13875.
[15] Wei M, Zhang J, Jia M, et al. α/β-Hydrolase domain-containing 6(ABHD6) negatively regulates the surface delivery and synaptic function of AMPA receptors[J]. Proc Natl Acad Sci,2016,113(19):E2695-2704.
[16] Jiang W, Wei M, Liu M, et al. The identification of protein tyrosine phosphatase receptor type O (PTPRO) as a synaptic adhesion molecule that promotes synapse formation[J]. J Neurosci,2017,37(41):9828-9843.
[17] Wei M, Jia M, Zhang J, et al. The inhibitory effect of α/β-hydrolase domain-containing 6(ABHD6) on the surface targeting of GluA2-and GluA3-containing AMPA receptors[J]. Front Mol Neurosci,2017,10:55.
[18] Yang X, Hou D, Jiang W, et al. Intercellular protein-protein interactions at synapses[J]. Protein Cell,2014,5(6):420-444.
[19] Zhang C, Atasoy D, Arac D, et al. Neurexins physically and functionally interact with GABAA receptors[J]. Neuron,2010,66(3):403-416.
[20] Zhang C, Milunsky, J M, Newton S, et al. A neuroligin-4 missense mutation associated with autism impairs neuroligin-4 folding and endoplasmic reticulum export[J]. J Neurosci,2009,29(35):10843-10854.
[21] Bao L, Jin S X, Zhang C, et al. Activation of delta opioid receptors induces receptor insertion and neuropeptide secretion[J]. Neuron, 2003,37(1):121-133.
[22] Wei M, Zhang J, Jia M, et al. α/β-Hydrolase domain-containing 6(ABHD6) negatively regulates the surface delivery and synaptic function of AMPA receptors[J]. Proc Natl Acad Sci,2016,113(19):E2695-E2704.
[23] Zhang C,Zhou Z. Ca(2+)-independent but voltage-dependent secretion in mammalian dorsal root ganglion neurons[J]. Nat Neurosci,2002,5(5):425-430.
[24] Zhang C, Xiong W, Zheng H, et al. Calcium-and dynamin-independent endocytosis in dorsal root ganglion neurons[J]. Neuron,2004, 42(2):225-236.