Motor Proteins and Their Role in Neuroinflammation and Neurodegeneration in Parkinson’s Disease

School Name

South Carolina Governor's School for Science and Mathematics

Grade Level

12th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder that causes the loss of dopaminergic neurons in the brain. My lab saw that calpain activation in PD may be linked to its degenerative characteristics. My study sought to track PD’s effect on neurons using the motor proteins Kinesin and Dynein, with the inhibition of Calpain. Kinesin mediates anterograde movement of cellular contents, and Dynein mediates retrograde movement of cellular contents. We stained VSC4.1 cells (neuronal cells) with the two motor proteins and Map2 (neuron-specific protein). Using these markers, I observed how the Calpain-2 inhibitor, zLLy, could prevent the loss of neurons against MPP⁺, a toxic metabolite derived from MPTP. When I experimented, I cultured four chambers of VSC4.1 (a motoneuronal cell line). I split the chamber into a control group (only cells), MPP⁺, MPP⁺ & zLLy, and zLLy. First, I plated the cells, then incubated them in CO₂ overnight for cell growth. Next, I added fresh media for the cells and changed it when needed. Finally, I added methanol and immunostained. Finally, I imaged with the electronic microscope. In my findings, the photos suggest that the inhibition of Calpain-2 prevents the loss of motor proteins. Also, my lab conducted experiments where PD can be seen in the spinal cord. To confirm my study with the neurons, I used spinal cord tissue treated with MPTP in mice. The data suggested that inhibition of all Calpain (using Calpeptin, a pan-calpain inhibitor) and Calpain-2 both helped in restoring motor proteins in the spinal cord.

Location

Furman Hall 106

Start Date

3-28-2026 11:15 AM

Presentation Format

Oral Only

Group Project

No

COinS
 
Mar 28th, 11:15 AM

Motor Proteins and Their Role in Neuroinflammation and Neurodegeneration in Parkinson’s Disease

Furman Hall 106

Parkinson’s disease (PD) is a neurodegenerative disorder that causes the loss of dopaminergic neurons in the brain. My lab saw that calpain activation in PD may be linked to its degenerative characteristics. My study sought to track PD’s effect on neurons using the motor proteins Kinesin and Dynein, with the inhibition of Calpain. Kinesin mediates anterograde movement of cellular contents, and Dynein mediates retrograde movement of cellular contents. We stained VSC4.1 cells (neuronal cells) with the two motor proteins and Map2 (neuron-specific protein). Using these markers, I observed how the Calpain-2 inhibitor, zLLy, could prevent the loss of neurons against MPP⁺, a toxic metabolite derived from MPTP. When I experimented, I cultured four chambers of VSC4.1 (a motoneuronal cell line). I split the chamber into a control group (only cells), MPP⁺, MPP⁺ & zLLy, and zLLy. First, I plated the cells, then incubated them in CO₂ overnight for cell growth. Next, I added fresh media for the cells and changed it when needed. Finally, I added methanol and immunostained. Finally, I imaged with the electronic microscope. In my findings, the photos suggest that the inhibition of Calpain-2 prevents the loss of motor proteins. Also, my lab conducted experiments where PD can be seen in the spinal cord. To confirm my study with the neurons, I used spinal cord tissue treated with MPTP in mice. The data suggested that inhibition of all Calpain (using Calpeptin, a pan-calpain inhibitor) and Calpain-2 both helped in restoring motor proteins in the spinal cord.