About Us

The Chung laboratory is interested in understanding how ion channels and their dynamic regulation modulate neuronal excitability, communications, and plasticity in the brain.

Ion channels are pore-forming proteins that generate electric current by mediating the flow of ions across the plasma membrane in morphologically and functionally distinct neuronal compartments called axons and dendrites. Axons generate and propagate action potentials whereas dendrites receive them at inter-cellular junctions called synapses where synaptic transmissions (communications) occur between neurons.

Ion channel dysregulation is involved in a wide variety of neurologic and neuropsychiatric diseases. In Chung lab, we focus on epilepsy and Alzheimer’s disease (AD).

Epilepsy is a common chronic brain disorder caused by excessive brain activity clinically characterized as seizures, which are abnormal and uncontrolled discharges of electrical signals in the brain cells called neurons. Drug-resistant seizures have severe consequences including cognitive decline, high mortality rate, psychiatric disorders, neurodevelopmental delay, and brain damage caused by surgical resection of seizure foci. Hence, better understanding of the pathogenesis of epilepsy is critical to develop novel therapeutic interventions and early diagnostics for epilepsy. A fundamental question is “how do neurons change themselves to produce excessive electrical signals in an epileptic brain compared to a normal brain?

The major goals of the Chung lab research in epilepsy have been to

(1) Understand how epilepsy mutations affect the function, neuronal localization, and surface density of voltage-gated potassium channels and lead to neuronal hyperactivity in inherited or de novo epilepsy

(2) Identify molecular mechanisms that persistently alter ion channels and their regulators to induce or alter neuronal plasticity and cause brain hyperactivity during the development of acquired epilepsy.

Alzheimer’s disease (AD) is the most common cause of dementia with 2 major pathological hallmarks: extracellular senile amyloid-b(Ab) plaques and intracellular neurofibrillary tangles (NFT) composed of hyperphosphorylated tau. Memory loss in the early stage of AD is associated with soluble Ab-mediated synaptic dysfunction before neurodegeneration is evident, whereas clinical dementia in AD is better correlated with neuronal loss and the formation of NFT. However, low or inconsistent clinical trials targeting Ab and tau necessitate new therapeutic drug targets and delivery methods.

The Chung lab has launched a new research in AD in collaboration with the Selvin and Kong labs in Physics and Chemical Engineering, respectively, to

(1) Understand soluble Ab and hyperphosphorylated tau affect glutamate receptors and potassium channels in the presence of Apolipoprotein-ԑ4 (ApoE4), the most prevalent genetic risk factor for AD,

(2) Test Dr. Kong’s novel nanoparticles as drug carriers to correct ApoE4 and alleviate synaptic dysfunction and  neuroinflammation in AD.

To investigate these important research themes, the Chung lab employs interdisciplinary approaches including molecular structure-function studies, microscopy, biochemistry, electrophysiology in primary neuronal culture, and mouse models.

Read more about our research in the IHSI blog post (https://blogs.illinois.edu/view/6761/717903).

***Illinois News Bureau on KCNQ/Kv7 research https://news.illinois.edu/view/6367/1884974120

***Illinois News Bureau on STEP research https://news.illinois.edu/view/6367/356876441

***Highlighted in MCB