University at Buffalo - The State University of New York
Skip to Content
Jian                           Feng

Jian Feng PhD

Department of Physiology and Biophysics


Specialty/Research Focus

Apoptosis and cell death; Cytoskeleton and cell motility; Gene Expression; Molecular and Cellular Biology; Molecular genetics; Neurobiology; Neurodegenerative disorders; Neurology; Pathophysiology; Protein Folding; Signal Transduction; Toxicology and Xenobiotics; Transcription and Translation

Professional Summary:

My research is aimed at finding the cause and a cure for Parkinson’s disease.

Parkinson’s disease (PD) is defined by a characteristic set of locomotor symptoms (rest tremor, rigidity, bradykinesia and postural instability) that are believed to be caused by the selective loss of dopaminergic (DA) neurons in substantia nigra. The persistent difficulties in using animals to model this human disease suggest that human nigral dopaminergic neurons have certain vulnerabilities that are unique to our species.

One of our unique features is the large size of the human brain (1350 grams on average) relative to the body. A single nigral dopaminergic neuron in a rat brain (2 grams) has a massive axon arbor with a total length of 45 centimeters. Assuming that all mammalian species share a similar brain wiring plan, we can estimate (using the cube root of brain weight) that a single human nigral dopaminergic neuron may have an axon with gigantic arborization that totals 4 meters.

Another unique feature of our species is our strictly bipedal movement, which is affected by Parkinson’s disease, in contrast to the quadrupedal movement of almost all other mammalian species. The much more unstable bipedal movement may require more dopamine, which supports the neural computation necessary for movement.

The landmark discovery of human induced pluripotent stem cells (iPSC) made it possible to generate patient-specific human midbrain dopaminergic neurons to study Parkinson’s disease. A key problem for dopaminergic neurons is the duality of dopamine as a signal required for neural computation and a toxin as its oxidation produces free radicals. Our study using iPSC-derived midbrain dopaminergic neurons from PD patients with parkin mutations and normal subjects shows that parkin sustains this necessary duality by maintaining the precision of the signal while suppressing the toxicity. Mutations of parkin cause increased spontaneous release of dopamine and reduced dopamine uptake, thereby disrupting the precision of dopaminergic transmission. On the other hand, transcription of monoamine oxidase is greatly increased when parkin is mutated. This markedly increases dopamine oxidation and oxidative stress. These phenomena have not been seen in parkin knockout mice, suggesting the usefulness of parkin-deficient iPSC-derived midbrain DA neurons as a cellular model for Parkinson’s disease.

Currently, we are using iPS cells and induced DA neurons to expand our studies on parkin to idiopathic Parkinson’s disease. We are also utilizing the molecular targets identified in our studies to find small-molecule compounds that can mimic the beneficial functions of parkin. The availability of human midbrain DA neurons should significantly speed up the discovery of a cure for Parkinson’s disease.

Education and Training:
  • PhD, Biochemistry, University of Tennessee (1997)
  • BS, Biochemistry, Nanjing University (1990)
  • Professor, Physiology and Biophysics, State University of New York at Buffalo (2010-present)
  • Associate Professor, Physiology and Biophysics, State University of New York at Buffalo (2005–2010)
  • Assistant Professor, Physiology and Biophysics, State University of New York at Buffalo (2000–2005)
  • Postdoctoral Research Associate, Laboratory of Molecular and Cellular Neuroscience, Rockefeller University (1997–2000)

Grants and Sponsored Research:
  • April 2017–March 2022
    A Novel Epigenetic Mechanism for Alzheimer's Disease
    Role: Co-Investigator
  • April 2014–March 2018
    Kinetic Barriers of Transdifferentiation
    Department of Veterans Affairs
    Role: Principal Investigator
  • June 2014–May 2017
    Understand the Pathophysiology of Parkinson's Disease Using Genetically Modified iPS Cells
    Role: Principal Investigator
  • March 2013–February 2016
    Redefining Idiopathic Parkinson’s Disease through Induced Pluriopotent Stem Cells
    Role: Principal Investigator
  • January 2009–December 2013
    Cellular Functions of Parkin
    Role: Principal Investigator

Journal Articles:
See all (34 more)

Service Activities:
  • Councilor, Society for Experimental Biology and Medicine; I serve as a Councilor at the Society for Experimental Biology and Medicine for the term of 2015-2019.; Councilor (2015–2019)

School News:
In the Media:

Clinical Specialties:
Clinical Offices:
Insurance Accepted:

Contact Information

549 Biomedical Research Building
Buffalo, NY 14214
Phone: (716) 829-2345
Fax: 716-829-2699

Log in to Update Your Profile