Hongjun Fu, PhD

Profile Headshot

Overview

Academic Appointments

  • Assistant Professor of Pathology & Cell Biology at CUMC

Languages

  • Chinese

Credentials & Experience

Education & Training

  • BS, 1999 Preventive Medicine, Anhui Medical University (China)
  • MS, 2002 Preventive Medicine, Sun Yat-Sen University of Medical Sciences (China)
  • PhD, 2007 Biochemistry, The Hong Kong University of Science and Technology, Hong Kong

Research

One of the fundamental questions common to all of the neurodegenerative diseases is why a particular disease targets specific neuronal populations? In early Alzheimer's disease (AD), distinct subgroups of neurons in layer II of the entorhinal cortex (EC) and the CA1 region of the hippocampus are particularly vulnerable to degeneration, while other cortical and hippocampal cell populations do not show pathological signs at this disease stage. Our research focuses on understanding which subtypes of neurons are vulnerable to tau pathology in early AD and other tauopathies as well as the molecular and cellular mechanisms underlying the selective neuronal vulnerability. In particular, we are interested in investigating the role of cell-autonomous (neurons) versus cell non-autonomous (microglia and/or astrocytes) effects as well as aging in selective vulnerability to proteinopathies in neurodegenerative diseases, specifically focusing on the ER proteostasis.

Research Interests

  • Selective neuronal vulnerability in early Alzheimer’s disease and other tauopathies
  • Role of ER stress in Alzheimer’s disease and other tauopathies
  • Role of microglial dysfunction in Alzheimer’s disease and other tauopathies

Grants

INVESTIGATING THE VULNERABILITY OF WFS1-EXPRESSING EXCITATORY NEURONS TO TAU PATHOLOGY IN EARLY ALZHEIMER S DISEASE. (Federal Gov)

Jul 15 2017 - Mar 31 2022

IDENTIFYING NEURONS VULNERABLE TO TAU PATHOLOGY IN EARLY AD (Private)

Apr 1 2017 - Mar 31 2020

PROPAGATION OF TAUOPATHY AND UPS DYSFUNCTION: IMPACT AND RESCUE WITH A UPS ACTIVATOR (Private)

Mar 1 2017 - Feb 28 2018

SPATIO TEMPORAL RELATIONSHIP OF PATHOLOGY AND FUNCTIONAL DECLINE WITH TAUOPATHY (Federal Gov)

Feb 1 2011 - Mar 31 2017

Selected Publications

Fu H*, Rodriguez GA*, Herman H, Emrani S, Nahmani E, Barrett G, Figueroa HY, Goldberg E, Hussaini SA*, Duff KE. Tau pathology induces excitatory neuron loss, grid cell dysfunction, and spatial memory deficits reminiscent of early Alzheimer's disease. Neuron 2017; 93(3):533-541.e5.

Fu H, Hussaini SA, Wegmann S, Profaci C, Daniels JD, Herman M, Emrani S, Figueroa HY, Hyman BT, Davies P, Duff KE. 3D visualization of the temporal and spatial spread of tau pathology reveals extensive sites of tau accumulation associated with neuronal loss and recognition memory deficit in aged tau transgenic mice. PLoS One, 2016; 11(7):e0159463.

Tosto G*, Fu H*, Vardarajan BN, Lee JH, Cheng R, Reyes-Dumeyer D, Lantigua R, Medrano M, Jimenez-Velazquez IZ, Elkind MS, Wright CB, Sacco RL, Pericak-Vance M, Farrer L, Rogaeva E, St George-Hyslop P, Reitz C, Mayeux R. F-box/LRR-repeat protein 7 is genetically associated with Alzheimer's disease. Ann Clin Transl Neurol 2015; 2:810-20.

Fu H, Liu B, Frost JL, Hong S, Jin M, Ostaszewski B, Shankar GM, Costantino IM, Carroll MC, Mayadas TN, Lemere CA. Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Abeta by microglia. Glia 2012; 60:993-1003.

Fu H*, Dou J*, Li W, Cui W, Mak S, Hu Q, Luo J, Lam CS, Pang Y, Youdim MB, Han Y. Promising multifunctional anti-Alzheimer's dimer bis(7)-Cognitin acting as an activator of protein kinase C regulates activities of alpha-secretase and BACE-1 concurrently. Eur J Pharmacol 2009; 623:14-21.

Fu H, Li W, Luo J, Lee NT, Li M, Tsim KW, Pang Y, Youdim MB, Han Y. Promising anti-Alzheimer’s dimer bis(7)-tacrine reduces b-amyloid generation by directly inhibiting BACE-1 activity. Biochem Biophys Res Commun 2008; 366:631-636.

Fu H, Dou J, Li W, Luo J, Li KC, Lam CS, Lee NT, Li M, Han Y. Mecamylamine prevents neuronal apoptosis induced by glutamate and low potassium via differential anticholinergic-independent mechanisms. Neuropharmacology 2008; 54:755-765.

Fu H, Li W, Liu Y, Lao Y, Liu W, Chen C, Yu H, Lee NT, Chang DC, Li P, Pang Y, Tsim KW, Li M, Han Y. Mitochondrial proteomic analysis and characterization of the intracellular mechanisms of bis(7)-tacrine in protecting against glutamate-induced excitotoxicity in primary cultured neurons. J Proteome Res 2007; 6:2435-2446.

Fu H, Li W, Lao Y, Luo J, Lee NT, Kan KK, Tsang HW, Tsim KW, Pang Y, Li Z, Chang DC, Li M, Han Y. Bis(7)-tacrine attenuates beta amyloid-induced neuronal apoptosis by regulating L-type calcium channels. J Neurochem 2006; 98:1400-1410.

Fu H, Hu QS, Lin ZN, Ren TL, Song H, Cai CK, Dong SZ. Aluminum-induced apoptosis in cultured cortical neurons and its effect on SAPK/JNK signal transduction pathway. Brain Research 2003; 980:11-23.