Neural activities are the basis of information representation and computation in the brain. While conventional tools in neuroscience can be effective in dissecting the brain circuits and neuronal subtypes involved in specific cognitive process, they provide limited insights in understanding the populational activities within a circuit. Therefore, a more refined set of tools in observing and manipulating neural activities can allow the investigation of principles of representation and computation of information in the brain. In my group, we combine the state-of-the-art in vivo microscopy and two-photon mediated single-cell gene editing/optogenetic technologies, in order to study the causal relationship of neural activity patterns and information coding during cognitive processes, and to establish and evaluate neural computation models at cellular level, thus advancing our understanding of brain functions.
Understanding the neural coding of cognitive variables and its abnormal state in brain disorders can provide invaluable insights in developing treatments against these conditions. In many brain disorders, the cognitive dysfunctions are not caused by neuronal death, but abnormalities in their firing patterns. Unfortunately, the link between the brain pathology and abnormal neural code is often poorly understood. Thus, rectifying neural code abnormalities remain to be an untapped opportunity for developing novel treatments, particularly for conditions that have been challenging due to the lack of obvious brain damage, such as autistic spectrum disorder, obsessive compulsive disorder and post-traumatic stress disorder.
Current project in my group:
1. Investigate the neural code of long-term memory and its abnormality in Alzheimer’s disease;
2. Investigate the neural code of short-term memory and explore its involvement in aphantasia;
3. Further develop novel tools for optical control of single-cell gene editing and optogenetics.
Email:pw_song@qq.com
Research Direction:观测阿尔茨海默症中的记忆信号
Email:23211520019@m.fudan.edu.cn
Research Direction:Functional investigation of neurovascular coupling
Email:ningd1@foxmail.com
Research Direction:印记细胞对长期记忆的编码
Email:18301050013@fudan.edu.cn
Research Direction:高维数据组分析
PLD3 affects axonal spheroids and network defects in Alzheimer’s disease. Yuan P, Zhang MY, Tong L, Morse T, McDougal R, Hui, D, Chan D, Yifei C, Grutzendler J. Nature, https://www.nature.com/articles/s41586-022-05491-6
Microglia constitute a barrier that prevents neurotoxic protofibrillar Aβ42 hotspots around plaques. Condello C#, Yuan P#, Schain A, Grutzendler J. Nature communications 6: 6176, 2015
Regional Blood Flow in the Normal and Ischemic Brain Is Controlled by Arteriolar Smooth Muscle Cell Contractility and Not by Capillary Pericytes. Hill RA#, Tong L#, Yuan P#, Murikinati S, Gupta S, Grutzendler J. Neuron 87(1): 95-110, 2015
Attenuation of β-amyloid deposition and neurotoxicity by chemogenetic modulation of neural activity. Yuan P, Grutzendler J. Journal of Neuroscience 36(2): 632-641, 2016
TREM2 haplodeficiency in mice and humans impairs the microglia barrier function leading to decreased amyloid compaction and severe axonal dystrophy. Yuan P, Condello C, Keene DC, Wang YM, Bird TD, Paul SM, Luo WJ, Colonna M, Baddeley D, Grutzendler J. Neuron 90: 724-739, 2016
RecV recombinase system for spatiotemporally controlled light-inducible genomic modifications. Yao SY#, Yuan P#, Ouellette B, Zhou T, Mortrud M, Balaram P, Chatterjee S, Wang Y, Daigle TL, Tasic B, Kuang XL, Gong H, Luo QM, Zeng SQ, Curtright A, Dhaka A, Kahan A, Gradinaru V, Chrapkiewicz R, Schnitzer M, Zeng HK, Cetin AH. Nature Method, 17: 422-429, 2020
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