Wei Lu-INSTITUTE FOR TRANSLATIONAL BRAIN RESEARCH

Wei Lu

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Wei Lu NSF Distinguished Young Scholars

Neural Plasticity and Memory

Dr. Wei Lu graduated with a bachelor’s degree in 1993 from Nanjing Medical University. He completed his Ph.D. in 1999 at Shanghai Medical University. He received his first postdoctoral training in the Department of Biology at Massachusetts Institute of Technology (MIT) and a second postdoc in the Department of Molecular and Cellular Biology (MCB) at Harvard University. Wei opened his lab in 2005 in the Department of Neurobiology at Nanjing Medical University and then moved to the School of Life Science and Technology at Southeast University. He is currently a Professor in the Institute of Translational Brain Research, Fudan University. Since 2005, the lab has received generous support from the National Natural Science Foundation of China (NSFC) and Ministry of Science and Technology of China (MOST). Wei’s group aims to elucidate four questions: 1) How is memory persistently maintained and stored? 2) How is remote memory retrieved? 3) How is recent memory consolidated into remote memory? 4) How dysfunctions of basal ganglion lead to various neuropsychiatric disorders, such as Parkinson’s disease (PD) and obsessive-compulsive disorder (OCD)? The long-term goal is to explore potential treatments for people with memory or movement disorders.

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Overview

Neural plasticity (neuroplasticity) refers to the phenomenon that the brain changes the efficacy of neural transmission in response to external activity or sensory inputs. This comprises plastic changes on both the functional and structural aspects and can occur at synaptic, cellular, circuitry and network levels. At present, it is widely considered that neural plasticity (especially at synapse level) shares similar cellular mechanism with memory processes. Moreover, abnormal neural plasticity plays critical roles in the occurrence and development of numerous neurodegenerative and psychiatric disorders. We are currently pursuing studies in two general project areas (outlined below).

Ongoing Research Projects

Project 1: Investigate the neural mechanisms underlying sustained storage and retrieval of remote memory.

Learning and memory are not only the basic functions for organisms to avoid danger and increase their adaptive fitness, but also are crucial for our own daily life. Prominent learning and memorizing abilities enable us to easily handle the intensive work schedule. It is also a growing attention in our healthcare, when we increasingly witness or worry about memory deficits such as Alzheimer’s disease (AD) or post-traumatic stress disorder (PTSD) among our friends and families. How can we stall the memory loss in Alzheimer’s patients? How can we enhance the extinction of the bad memory on trauma? Solving these problems would rely on decrypting basic operating principle of memory processes in our brain. Our most dedicated research interest is to decipher the structural and molecular substrate for remote memory, which can be persistently maintained and stored. Specific questions we are trying to address include: Where and how is remote memory stored? How is recent memory consolidated into remote memory? How is remote memory retrieved? We are now employing immunochemistry, electrophysiology, fluorescence imaging, optogenetics, viral tracing and behavioral assays etc. to investigate these questions. The ongoing projects aim to elucidate:

(1) Cortical microcircuits for remote memory retrieval;

(2) Microcircuits related to the storage and retrieval of remote memory;

(3) How memory is transferred from hippocampus to cortex during consolidation;

(4) How is the stubborn pathological memory formed in PTSD.

Project 2: Investigate the neural mechanisms underlying various brain disorders related to dysfunction of basal ganglia, such as Parkinson’s disease (PD) and obsessive-compulsive disorder (OCD), and exploration of potential neuromodulation treatments for people with movement disorders.

PD is a neurodegenerative motor disorder. Its core symptoms include bradykinesia and tremors. Deep brain stimulus (DBS) has become a major treatment in late-stage development of this disease. However, due to lacking of understanding on the mechanism underlying DBS’s efficacy, we are not able to further optimize stimulation protocols to improve its effects in some patients. One potential solution to this problem is to find a unique electrophysiological marker for motor deficits in PD and refine DBS protocol to better target occurrence of motion inability. We are currently focusing on the phenomenon of increased beta oscillations in basal ganglia and other brain regions. We hope to pinpoint the initial occurring region of this abnormality, find the local circuitry basis behind its generation and the spreading mechanisms behind this oscillatory activity. In addition, when multiple brain regions demonstrate such abnormal oscillations, their local field potential tend to exhibit a phenomenon of over-synchronization. How does such over-synchronization arise? Are motor deficits related to this phenomenon? These are all scientific questions we are striving to answer. Through answering these questions, we hope to provide new guidelines in setting electrical parameters in DBS protocols. Recently, we also focused on one of the core symptoms shared by OCD and Autism’s spectrum disorder (ASD): compulsory repetitive behavior. In animal models, this manifests as over-grooming behavior. We are discovering and analyzing neuronal circuits underlying the generation and modulation of this behavior. The ongoing projects aim to elucidate:

(1) The correlation between excessive beta synchronization at basal ganglion regional and motor deficits in PD;

(2) Electrophysiological markers for PD prodromal diagnosis;

(3) Neural mechanisms underlying generation of repetitive behaviors in OCD;

(4) Novel neuromodulation treatment for people with movement disorders.