Yadong Huang and his team focus on the causes and progression of Alzheimer’s disease. Specifically, they study a variant of apolipoprotein E, called apolipoprotein E4 (apoE4). Approximately 60–75 percent of Alzheimer’s patients carry the apoE4 variant, making it the most important genetic risk factor for Alzheimer’s disease. The team uses mouse models and induced pluripotent stem (iPS) cells made from skin cells of patients carrying apoE4 or other mutations related to Alzheimer’s to study their effects on the development, survival, and degeneration of neurons. In addition, Huang’s lab is working to identify drug targets and develop therapeutic strategies for Alzheimer’s disease and other neurodegenerative disorders.
Areas of Expertise
Huang’s group has made important contributions to understanding how apoE4 causes neuronal deficits and cognitive decline in Alzheimer’s disease. Using a mouse model, they showed that human apoE4 is expressed in neurons and causes age-dependent learning and memory impairments, as well as degeneration of GABAergic interneurons in the dentate gyrus, a brain region involved in learning and memory. They also discovered that mice with apoE4 have deficits in hippocampal network activities called sharp-wave ripples, which indicates that a decline of interneuron-enabled slow gamma activity during sharp-wave ripples contributes to apoE4-mediated learning and memory impairments.
The second major effort in Huang’s lab has been to develop better drugs for Alzheimer’s disease. Using human neurons derived from iPS cells, the group demonstrated that those harboring apoE4 have higher levels of tau phosphorylation, increased amyloid beta production, and increased risk of degeneration especially when differentiated into GABAergic interneurons. Huang and his team showed that treating apoE4 neurons with a small-molecule structure corrector ameliorated the detrimental effects, suggesting that correcting the pathogenic conformation of apoE4 is a viable therapeutic approach for apoE4-related Alzheimer’s disease.
Senior Investigator, Gladstone Institutes
Director, Center for Translational Advancement, Gladstone Institutes
Investigator, Roddenberry Stem Cell Center, Gladstone Institutes
Professor of Neurology and Pathology, UC San Francisco
Yadong Huang, MD, PhD, is a senior investigator at Gladstone Institutes, where he is also the director of the Center for Translational Advancement and an investigator in the Roddenberry Stem Cell Center. In addition, he is a professor of neurology and pathology at UC San Francisco.
He earned an MD from Qingdao Medical University in China, and a PhD in biochemistry and pathology from Peking Union Medical College and Chinese Academy of Medical Sciences in Beijing. He was trained as a postdoctoral fellow at the Arteriosclerosis Research Institute at the University of Muenster, Germany. Huang joined Gladstone Institutes in 1995 as a postdoctoral fellow, and became a staff research investigator in 1999. In 2015, he was promoted to senior investigator.
Huang studies the pathogenesis of Alzheimer’s disease, focusing on the roles of apoE4. His laboratory demonstrates that apoE4 is expressed in neurons where it is proteolytically cleaved, leading to the generation of neurotoxic fragments that contribute to Alzheimer’s disease. His laboratory also showed that expression of apoE4 causes age-dependent impairment of GABAergic interneurons in the hippocampus, leading to learning and memory deficits. He has been heavily involved in identifying strategies for the treatment or prevention of Alzheimer’s disease by targeting apoE4. Huang has published more than 120 scientific papers. He is a scientific co-founder for two pharmaceutic companies: E-Scape Bio, Inc. and GABAeron, Inc.
Why Are You Dedicated to Discovery
“I am driven to understanding the molecular basis of Alzheimer’s and other brain diseases using genetics, pharmacological drugs, mouse models, stem cells—any means available to study and treat these devastating diseases.”
Honors and Awards
2000 Young Investigator Award for Scientific Excellence, International Society for Atherosclerosis Research
1996 Young Investigator Award, XII International Symposium on Drugs Affecting Lipid Metabolism
1995 W.H. Hauss Award on Atherosclerosis Research, German Arteriosclerosis Research Society
- Small-molecule structure correctors target abnormal protein structure and function: structure corrector rescue of apolipoprotein E4-associated neuropathology. Mahley RW, Huang Y. J Med Chem. 2012 Nov 08; 55(21):8997-9008.
- Arf4 determines dentate gyrus-mediated pattern separation by regulating dendritic spine development. PLoS One Jain S, Yoon SY, Zhu L, Brodbeck J, Dai J, Walker D, Huang Y. . 2012; 7(9):e46340.
- Hilar GABAergic interneuron activity controls spatial learning and memory retrieval. Andrews-Zwilling Y, Gillespie AK, Kravitz AV, Nelson AB, Devidze N, Lo I, Yoon SY, Bien-Ly N, Ring K, Zwilling D, Potter GB, Rubenstein JL, Kreitzer AC, Huang Y. PLoS One. 2012; 7(7):e40555.
- Direct reprogramming of mouse and human fibroblasts into multipotent neural stem cells with a single factor. Ring KL, Tong LM, Balestra ME, Javier R, Andrews-Zwilling Y, Li G, Walker D, Zhang WR, Kreitzer AC, Huang Y. Cell Stem Cell. 2012 Jul 06; 11(1):100-9.
- ApoE and TDP-43 neuropathology in two siblings with familial FTLD-motor neuron disease. Vossel KA, Bien-Ly N, Bernardo A, Rascovsky K, Karydas A, Rabinovici GD, Sidhu M, Huang EJ, Miller BL, Huang Y, Seeley WW. Neurocase. 2013; 19(3):295-301.
- Reducing human apolipoprotein E levels attenuates age-dependent Aß accumulation in mutant human amyloid precursor protein transgenic mice. Bien-Ly N, Gillespie AK, Walker D, Yoon SY, Huang Y. J Neurosci. 2012 Apr 04; 32(14):4803-11.
- Alzheimer mechanisms and therapeutic strategies. Huang Y, Mucke L. Cell. 2012 Mar 16; 148(6):1204-22.
- Small molecule structure correctors abolish detrimental effects of apolipoprotein E4 in cultured neurons. Chen HK, Liu Z, Meyer-Franke A, Brodbeck J, Miranda RD, McGuire JG, Pleiss MA, Ji ZS, Balestra ME, Walker DW, Xu Q, Jeong DE, Budamagunta MS, Voss JC, Freedman SB, Weisgraber KH, Huang Y, Mahley RW. J Biol Chem. 2012 Feb 17; 287(8):5253-66.
- Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimer's disease: lessons from ApoE mouse models. Huang Y. Biochem Soc Trans. 2011 Aug; 39(4):924-32.
- Kynurenine 3-monooxygenase inhibition in blood ameliorates neurodegeneration. Zwilling D, Huang SY, Sathyasaikumar KV, Notarangelo FM, Guidetti P, Wu HQ, Lee J, Truong J, Andrews-Zwilling Y, Hsieh EW, Louie JY, Wu T, Scearce-Levie K, Patrick C, Adame A, Giorgini F, Moussaoui S, Laue G, Rassoulpour A, Flik G, Huang Y, Muchowski JM, Masliah E, Schwarcz R, Muchowski PJ. Cell. 2011 Jun 10; 145(6):863-74.
- Structure-dependent impairment of intracellular apolipoprotein E4 trafficking and its detrimental effects are rescued by small-molecule structure correctors. Brodbeck J, McGuire J, Liu Z, Meyer-Franke A, Balestra ME, Jeong DE, Pleiss M, McComas C, Hess F, Witter D, Peterson S, Childers M, Goulet M, Liverton N, Hargreaves R, Freedman S, Weisgraber KH, Mahley RW, Huang Y. J Biol Chem. 2011 May 13; 286(19):17217-26.
- C-terminal-truncated apolipoprotein (apo) E4 inefficiently clears amyloid-beta (Abeta) and acts in concert with Abeta to elicit neuronal and behavioral deficits in mice. Bien-Ly N, Andrews-Zwilling Y, Xu Q, Bernardo A, Wang C, Huang Y. Proc Natl Acad Sci U S A. 2011 Mar 08; 108(10):4236-41.
- Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease. Chen HK, Ji ZS, Dodson SE, Miranda RD, Rosenblum CI, Reynolds IJ, Freedman SB, Weisgraber KH, Huang Y, Mahley RW. J Biol Chem. 2011 Feb 18; 286(7):5215-21.
- Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice. Andrews-Zwilling Y, Bien-Ly N, Xu Q, Li G, Bernardo A, Yoon SY, Zwilling D, Yan TX, Chen L, Huang Y. J Neurosci. 2010 Oct 13; 30(41):13707-17.
- Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases. Huang Y. Curr Opin Lipidol. 2010 Aug; 21(4):337-45.
- Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice. Buttini M, Masliah E, Yu GQ, Palop JJ, Chang S, Bernardo A, Lin C, Wyss-Coray T, Huang Y, Mucke L. Am J Pathol. 2010 Aug; 177(2):563-9.
- Abeta-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease. Huang Y. Trends Mol Med. 2010 Jun; 16(6):287-94.
- GABAergic interneuron dysfunction impairs hippocampal neurogenesis in adult apolipoprotein E4 knockin mice. Li G, Bien-Ly N, Andrews-Zwilling Y, Xu Q, Bernardo A, Ring K, Halabisky B, Deng C, Mahley RW, Huang Y. Cell Stem Cell. 2009 Dec 04; 5(6):634-45.
- Bioactive TGF-beta can associate with lipoproteins and is enriched in those containing apolipoprotein E3. Tesseur I, Zhang H, Brecht W, Corn J, Gong JS, Yanagisawa K, Michikawa M, Weisgraber K, Huang Y, Wyss-Coray T. J Neurochem. 2009 Aug; 110(4):1254-62.
- Alzheimer disease: multiple causes, multiple effects of apolipoprotein E4, and multiple therapeutic approaches. Mahley RW, Huang Y. Ann Neurol. 2009 Jun; 65(6):623-5.
- Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS. Mahley RW, Weisgraber KH, Huang Y. J Lipid Res. 2009 Apr; 50 Suppl:S183-8.
- Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates HIV disease progression. Burt TD, Agan BK, Marconi VC, He W, Kulkarni H, Mold JE, Cavrois M, Huang Y, Mahley RW, Dolan MJ, McCune JM, Ahuja SK. Proc Natl Acad Sci U S A. 2008 Jun 24; 105(25):8718-23.
- Intron-3 retention/splicing controls neuronal expression of apolipoprotein E in the CNS. Xu Q, Walker D, Bernardo A, Brodbeck J, Balestra ME, Huang Y. J Neurosci. 2008 Feb 06; 28(6):1452-9.
- Rosiglitazone increases dendritic spine density and rescues spine loss caused by apolipoprotein E4 in primary cortical neurons. Brodbeck J, Balestra ME, Saunders AM, Roses AD, Mahley RW, Huang Y. Proc Natl Acad Sci U S A. 2008 Jan 29; 105(4):1343-6.
- Detrimental effects of apolipoprotein E4: potential therapeutic targets in Alzheimer's disease. Mahley RW, Huang Y, Weisgraber KH. Curr Alzheimer Res. 2007 Dec; 4(5):537-40.
- Atherogenic remnant lipoproteins: role for proteoglycans in trapping, transferring, and internalizing. Mahley RW, Huang Y. J Clin Invest. 2007 Jan; 117(1):94-8.
- Molecular and cellular mechanisms of apolipoprotein E4 neurotoxicity and potential therapeutic strategies. Huang Y. Curr Opin Drug Discov Devel. 2006 Sep; 9(5):627-41.
- Complex disease-associated pharmacogenetics: drug efficacy, drug safety, and confirmation of a pathogenetic hypothesis (Alzheimer's disease). Roses AD, Saunders AM, Huang Y, Strum J, Weisgraber KH, Mahley RW. Pharmacogenomics J. 2007 Feb; 7(1):10-28.
- Profile and regulation of apolipoprotein E (ApoE) expression in the CNS in mice with targeting of green fluorescent protein gene to the ApoE locus. Xu Q, Bernardo A, Walker D, Kanegawa T, Mahley RW, Huang Y. J Neurosci. 2006 May 10; 26(19):4985-94.
- Putting cholesterol in its place: apoE and reverse cholesterol transport. Mahley RW, Huang Y, Weisgraber KH. J Clin Invest. 2006 May; 116(5):1226-9.
- Commentary on "Perspective on a pathogenesis and treatment of Alzheimer's disease." Apolipoprotein E and the mitochondrial metabolic hypothesis. Huang Y, Mahley RW. Alzheimers Dement. 2006 Apr; 2(2):71-3.
- Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease. Mahley RW, Weisgraber KH, Huang Y. Proc Natl Acad Sci U S A. 2006 Apr 11; 103(15):5644-51.
- Apolipoprotein E and Alzheimer disease. Huang Y. Neurology. 2006 Jan 24; 66(2 Suppl 1):S79-85.
- Apolipoprotein (apo) E4 and Alzheimer's disease: unique conformational and biophysical properties of apoE4 can modulate neuropathology. Mahley RW, Huang Y. Acta Neurol Scand Suppl. 2006; 185:8-14.
- Apolipoprotein (apo) E4 enhances amyloid beta peptide production in cultured neuronal cells: apoE structure as a potential therapeutic target. Ye S, Huang Y, Müllendorff K, Dong L, Giedt G, Meng EC, Cohen FE, Kuntz ID, Weisgraber KH, Mahley RW. Proc Natl Acad Sci U S A. 2005 Dec 20; 102(51):18700-5.
- Lipid- and receptor-binding regions of apolipoprotein E4 fragments act in concert to cause mitochondrial dysfunction and neurotoxicity. Chang S, ran Ma T, Miranda RD, Balestra ME, Mahley RW, Huang Y. Proc Natl Acad Sci U S A. 2005 Dec 20; 102(51):18694-9.
- Reactivity of apolipoprotein E4 and amyloid beta peptide: lysosomal stability and neurodegeneration. Ji ZS, Müllendorff K, Cheng IH, Miranda RD, Huang Y, Mahley RW. J Biol Chem. 2006 Feb 03; 281(5):2683-92.
- Effect of domain interaction on apolipoprotein E levels in mouse brain. Ramaswamy G, Xu Q, Huang Y, Weisgraber KH. J Neurosci. 2005 Nov 16; 25(46):10658-63.
- Apolipoprotein A-V: a potential modulator of plasma triglyceride levels in Turks. Hodoglugil U, Tanyolaç S, Williamson DW, Huang Y, Mahley RW. J Lipid Res. 2006 Jan; 47(1):144-53.
- Common polymorphisms of ATP binding cassette transporter A1, including a functional promoter polymorphism, associated with plasma high density lipoprotein cholesterol levels in Turks. Hodoglugil U, Williamson DW, Huang Y, Mahley RW. Atherosclerosis. 2005 Dec; 183(2):199-212.
- Increased tau phosphorylation in apolipoprotein E4 transgenic mice is associated with activation of extracellular signal-regulated kinase: modulation by zinc. Harris FM, Brecht WJ, Xu Q, Mahley RW, Huang Y. J Biol Chem. 2004 Oct 22; 279(43):44795-801.
- ApoE genotype accounts for the vast majority of AD risk and AD pathology. Raber J, Huang Y, Ashford JW. Neurobiol Aging. 2004 May-Jun; 25(5):641-50.
- Apolipoprotein E4 domain interaction occurs in living neuronal cells as determined by fluorescence resonance energy transfer. Xu Q, Brecht WJ, Weisgraber KH, Mahley RW, Huang Y. J Biol Chem. 2004 Jun 11; 279(24):25511-6.
- Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice. Brecht WJ, Harris FM, Chang S, Tesseur I, Yu GQ, Xu Q, Dee Fish J, Wyss-Coray T, Buttini M, Mucke L, Mahley RW, Huang Y. J Neurosci. 2004 Mar 10; 24(10):2527-34.
- Apolipoprotein E: diversity of cellular origins, structural and biophysical properties, and effects in Alzheimer's disease. Huang Y, Weisgraber KH, Mucke L, Mahley RW. J Mol Neurosci. 2004; 23(3):189-204.
- Astroglial regulation of apolipoprotein E expression in neuronal cells. Implications for Alzheimer's disease. Harris FM, Tesseur I, Brecht WJ, Xu Q, Mullendorff K, Chang S, Wyss-Coray T, Mahley RW, Huang Y. J Biol Chem. 2004 Jan 30; 279(5):3862-8.
- Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice. Harris FM, Brecht WJ, Xu Q, Tesseur I, Kekonius L, Wyss-Coray T, Fish JD, Masliah E, Hopkins PC, Scearce-Levie K, Weisgraber KH, Mucke L, Mahley RW, Huang Y. Proc Natl Acad Sci U S A. 2003 Sep 16; 100(19):10966-71.
- Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formation. Buttini M, Yu GQ, Shockley K, Huang Y, Jones B, Masliah E, Mallory M, Yeo T, Longo FM, Mucke L. J Neurosci. 2002 Dec 15; 22(24):10539-48.
- Evidence for differential effects of apoE3 and apoE4 on HDL metabolism. Hopkins PC, Huang Y, McGuire JG, Pitas RE. J Lipid Res. 2002 Nov; 43(11):1881-9.
- Apolipoprotein E4 potentiates amyloid beta peptide-induced lysosomal leakage and apoptosis in neuronal cells. Ji ZS, Miranda RD, Newhouse YM, Weisgraber KH, Huang Y, Mahley RW. J Biol Chem. 2002 Jun 14; 277(24):21821-8.
- Apolipoprotein E fragments present in Alzheimer's disease brains induce neurofibrillary tangle-like intracellular inclusions in neurons. Huang Y, Liu XQ, Wyss-Coray T, Brecht WJ, Sanan DA, Mahley RW. Proc Natl Acad Sci U S A. 2001 Jul 17; 98(15):8838-43.
- Endogenous apolipoprotein E modulates cholesterol efflux and cholesteryl ester hydrolysis mediated by high-density lipoprotein-3 and lipid-free apolipoproteins in mouse peritoneal macrophages. Langer C, Huang Y, Cullen P, Wiesenhütter B, Mahley RW, Assmann G, von Eckardstein A. J Mol Med (Berl). 2000; 78(4):217-27.
- Overexpression of apolipoprotein E3 in transgenic rabbits causes combined hyperlipidemia by stimulating hepatic VLDL production and impairing VLDL lipolysis. Huang Y, Ji ZS, Brecht WJ, Rall SC, Taylor JM, Mahley RW. Arterioscler Thromb Vasc Biol. 1999 Dec; 19(12):2952-9.
- Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia). Questions, quandaries, and paradoxes. Mahley RW, Huang Y, Rall SC. J Lipid Res. 1999 Nov; 40(11):1933-49.
- Apolipoprotein E: from atherosclerosis to Alzheimer's disease and beyond. Mahley RW, Huang Y. Curr Opin Lipidol. 1999 Jun; 10(3):207-17.
- Overexpression and accumulation of apolipoprotein E as a cause of hypertriglyceridemia. Huang Y, Liu XQ, Rall SC, Taylor JM, von Eckardstein A, Assmann G, Mahley RW. J Biol Chem. 1998 Oct 09; 273(41):26388-93.
- Apolipoprotein E2 reduces the low density lipoprotein level in transgenic mice by impairing lipoprotein lipase-mediated lipolysis of triglyceride-rich lipoproteins. Huang Y, Liu XQ, Rall SC, Mahley RW. J Biol Chem. 1998 Jul 10; 273(28):17483-90.
- Increased expression of apolipoprotein E in transgenic rabbits results in reduced levels of very low density lipoproteins and an accumulation of low density lipoproteins in plasma. Fan J, Ji ZS, Huang Y, de Silva H, Sanan D, Mahley RW, Innerarity TL, Taylor JM. J Clin Invest. 1998 May 15; 101(10):2151-64.
- Lipid-free apolipoprotein (apo) A-I is converted into alpha-migrating high density lipoproteins by lipoprotein-depleted plasma of normolipidemic donors and apo A-I-deficient patients but not of Tangier disease patients. von Eckardstein A, Huang Y, Kastelein JJ, Geisel J, Real JT, Kuivenhoven JA, Miccoli R, Noseda G, Assmann G. Atherosclerosis. 1998 May; 138(1):25-34.
- Genetic factors precipitating type III hyperlipoproteinemia in hypolipidemic transgenic mice expressing human apolipoprotein E2. Huang Y, Rall SC, Mahley RW. Arterioscler Thromb Vasc Biol. 1997 Nov; 17(11):2817-24.
- Effects of genotype and diet on cholesterol efflux into plasma and lipoproteins of normal, apolipoprotein A-I-, and apolipoprotein E-deficient mice. Huang Y, Zhu Y, Langer C, Raabe M, Wu S, Wiesenhütter B, Seedorf U, Maeda N, Assmann G, von Eckardstein A. Arterioscler Thromb Vasc Biol. 1997 Oct; 17(10):2010-9.
- Apolipoprotein E2 transgenic rabbits. Modulation of the type III hyperlipoproteinemic phenotype by estrogen and occurrence of spontaneous atherosclerosis. Huang Y, Schwendner SW, Rall SC, Sanan DA, Mahley RW. J Biol Chem. 1997 Sep 05; 272(36):22685-94.
- A natural apolipoprotein A-I variant, apoA-I (L141R)Pisa, interferes with the formation of alpha-high density lipoproteins (HDL) but not with the formation of pre beta 1-HDL and influences efflux of cholesterol into plasma. Miccoli R, Zhu Y, Daum U, Wessling J, Huang Y, Navalesi R, Assmann G, von Eckardstein A. J Lipid Res. 1997 Jun; 38(6):1242-53.
- Hypolipidemic and hyperlipidemic phenotypes in transgenic mice expressing human apolipoprotein E2. Huang Y, Schwendner SW, Rall SC, Mahley RW. J Biol Chem. 1996 Nov 15; 271(46):29146-51.
- High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. The PROCAM experience and pathophysiological implications for reverse cholesterol transport. Assmann G, Schulte H, von Eckardstein A, Huang Y. Atherosclerosis. 1996 Jul; 124 Suppl:S11-20.
- Phospholipid transfer protein mediated conversion of high density lipoproteins generates pre beta 1-HDL. von Eckardstein A, Jauhiainen M, Huang Y, Metso J, Langer C, Pussinen P, Wu S, Ehnholm C, Assmann G. Biochim Biophys Acta. 1996 Jun 11; 1301(3):255-62.
- Uptake, transfer, and esterification of cell-derived cholesterol in plasma of patients with familial HDL-deficiency. von Eckardstein A, Huang Y, Wu S, Assmann G. Z Gastroenterol. 1996 Jun; 34 Suppl 3:143-4.
- Effects of the apolipoprotein E polymorphism on uptake and transfer of cell-derived cholesterol in plasma. Huang Y, von Eckardstein A, Wu S, Assmann G. J Clin Invest. 1995 Dec; 96(6):2693-701.
- Generation of pre-beta 1-HDL and conversion into alpha-HDL. Evidence for disturbed HDL conversion in Tangier disease. Huang Y, von Eckardstein A, Wu S, Langer C, Assmann G. Arterioscler Thromb Vasc Biol. 1995 Oct; 15(10):1746-54.
- Lipoproteins containing apolipoprotein A-IV but not apolipoprotein A-I take up and esterify cell-derived cholesterol in plasma. von Eckardstein A, Huang Y, Wu S, Sarmadi AS, Schwarz S, Steinmetz A, Assmann G. Arterioscler Thromb Vasc Biol. 1995 Oct; 15(10):1755-63.
- Cholesterol efflux, cholesterol esterification, and cholesteryl ester transfer by LpA-I and LpA-I/A-II in native plasma. Huang Y, von Eckardstein A, Wu S, Assmann G. Arterioscler Thromb Vasc Biol. 1995 Sep; 15(9):1412-8.
- Reverse cholesterol transport in plasma of patients with different forms of familial HDL deficiency. von Eckardstein A, Huang Y, Wu S, Funke H, Noseda G, Assmann G. Arterioscler Thromb Vasc Biol. 1995 May; 15(5):691-703.
- Physiological role and clinical relevance of high-density lipoprotein subclasses. von Eckardstein A, Huang Y, Assmann G. Curr Opin Lipidol. 1994 Dec; 5(6):404-16.
- A plasma lipoprotein containing only apolipoprotein E and with gamma mobility on electrophoresis releases cholesterol from cells. Huang Y, von Eckardstein A, Wu S, Maeda N, Assmann G. Proc Natl Acad Sci U S A. 1994 Mar 01; 91(5):1834-8.
- Cell-derived unesterified cholesterol cycles between different HDLs and LDL for its effective esterification in plasma. Huang Y, von Eckardstein A, Assmann G. Arterioscler Thromb. 1993 Mar; 13(3):445-58.